Dr, Abdulraouf Abdullatif

Rheumatology

*Diseases which affect any joint inside the body.

*Classification: Inflammatory & Non- Inflammatory

Inflammatory

1/Rh-factor

Sero (+ve): Sero (-ve): HLA,B-27

1/R.A. *** 1/Ankylosing spondylitis.

2/SLE. *** 2/Psoriatic arthritis.

3/ Scleroderma. 3/ Reactive arthritis.

(Progressive systemic sclerosis)
4/Sclerotic Arthritis.
4/Sjogren Syndrome.
5/IBD Arthritis.
5/polymyositis .
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Dr, Abdulraouf Abdullatif

2/ Crystal Arthropathy: Gout & Pseudo gout. ***

3/Vacuities Syndrome:

a) Behest’s disease.
b) Giant cell arteritis.
c) Polymyalgia rheumatic.
d) Wagner’s granulomatosis : [c- ANCA +ve]
1/ Otits media

+Pulmonary nodules 50%

2/Upper airway involvement: 3/proptosis.

[Epistaxiss … hemoptysis … mucosal ulceration]

4/ Septic Arthritis

1) Rheumatoid Arthritis

Def: Chronic relapsing & remitting of poly-

arthicular Synovitis (affect synovial membrane) lead

to erosive synovitis of small joints mostly

affect hand and feet .

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Dr, Abdulraouf Abdullatif

Pathopysiology:
Destructive Synovitis.(Inf- mediators AUTOIMMUNE Causing erosion of synovial membrane no
synovial fluid irritation and hypertrophy of cartilage  joint space , small amount of effusion
began to form but not filling the space of joint b\c of thickening  escaping of fluid & swilling .

Hypertrophy is a good media for 2ry osteoarthritis  calcification  destruction  Ankylosis

(fusion of two articular surfaces)  stiffness  deformity.

Causes: most likely autoimmune b\c :

1) Female > male 3:1

2 Incidence (30-50yrs) middle aged. ( Age 

appears of deformity).

3) +ve F\H mostly father tree.

4) Genetic predisposition HALA Dr4 & Dr1

*the Abs that can be found

a) Rheumatoid factor, Most sensitive , high in blood (70-80%) was +ve, but
low specific. ‫ٌظهر فً اكثر من مرض‬

b) CCB antibody, (Cyclic citrullinated Peptide) which is highly specific & low
sensitive 30% find in blood.
, ‫مش كل الحاالت بٌظهرلك‬
low sensitive ‫لذلك هو‬

Theories:
*Inflammatory condition b\c, at acute stage the blood full with interleukins and cytokines.

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Dr, Abdulraouf Abdullatif

*Has high effect with smoking (Active & passive) and should relate also with genetic
predisposition.

Clinical Picture:

*Arthicular & Extra arthicular (b\c, escaping of inflammatory med to

circulation)
1) Arthicular:
manifestations (Most common presentation):

As mentioned above its polyarthicular affected mostly small joints

a) Arthritis : ‫فً شروط الزم توافرها‬

1\ Symmetrical .‫مش شرط فً نفس الوقت‬
2\ Non migratory (irreversible ) .
3\ Erosive. 4\polyarthicular synovitis > 2-3 joints.

Mainly affected joints of hands:

1) Wrist, which the most common joint affected.

2) Proximal interphalangeal joints.

All hand joints affected except

3) Metacarpophalangeal joint. Distal phalangeal J  b\c its not synovial type.

4) Metatarsophalangeal joint.

5) Ankle. 6) Knee. 7) Elbow. 8) Shoulder. 9) Hip (last

affected), may missed with postmenopausal arthritis.

N.B: The only non synovial joint affected is Atlanto Axial Joint at C1-C2 Due to an
inflammation of its tendons sliding of vertebrae Sublaxation spinal cord Compression
Paresthesia & Tingling of Upper limb  C\I any maneuver by neck extension b\c  Generalized

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Dr, Abdulraouf Abdullatif

paralysis death. Examples of neck extension maneuvers, [General anesthesia, Intubation

laryngoscope, endoscope & cranial nerve IX Examination].

b) Pain: mostly ass’ with tenderness, this pain usually at early

morning more than 1hr & then subsided b\c during sleepiness
there stasis b\c no movement and the swelling Obstruction of
the lymphatic system so , Inflammatory med. Increasing And
accumulated, lead to irritation and pain, but by movement 

drainage of mediators which leads to disappearing and subsides

the pain.

c) Swelling: inside the joint it indicates an active disease, but not

related with redness, maybe redness not caused by R.A caused
as 2ry complication (Trauma..Septic arthritis..Gouty in leg)
Joint swilling with infection and redness, the 1st aid of management is early aspiration
(Arthrocentesis), if neglected will cause a permanent damage of joint (septic arthritis )& coverage
with Abc &Analgesia & rehabilitation.

d) Muscle wasting & deformity: most cardinal feature

Disease which is relapsing and remitting and more likely to be
exposed to chronic  Msc wasting, causes:
1/nerve compression (median nerve which supplies thenar Msc)
compartment syndrome Rx by Fsciotomy.
2/myositis, (Arthritis Tendinitis  myositis) Erosion of wrist 
edemacompression
3/disused of Muscles (active disease)  wasting. on carpal canal, which
passes a median nerve
inside  carpal tunnel
synd loss of sense of
Lat 3.5 fingers
5 paresthesia at night
Dr, Abdulraouf Abdullatif

Deformity: the best indicator for chronisty & uncontrole

Deformity due to destruction of joints (small) & most common

Wrist joint.

1) Wrist joint:

*Erosion of radio styloid process  radial deviation

(decrease space).

*piano key deformity: sublaxation of Radial styloid

process (wrist drop).

2) Metacarpal phalangeal joint:

*ulnar deviation, due to destruction of 4th & 5th

Tendons  tendinitis  destruction.

*Pop up deformity, Sublaxation metacarpal phalangeal joint.

*Z-deformity of the thumb, flexion of metacarpal & extension of

interphalangeal joints.

3) Proximal interphalangeal joint:

* Swan neck deformity, extension of proximal interphalangeal &

Flexion of Distal interphalangeal (distal not affected but its mechanical deformity).

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Dr, Abdulraouf Abdullatif

*Boutonniere deformity, extension of distal & flexion of proximal.

N.B: Looking for scar’s surgery at medial & lateral aspects of hand,
which is an indicator for a chronosity.

4) Metatarsal phalyngeal joint: 

hummer toe deformity

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Dr, Abdulraouf Abdullatif

e) Baker’s Cyst : bulgy it occurs in pts with knee synovitis , &

synovial fluid accumulate in the cyst  Rupture  fluid escaping
to posterior compartment of leg  unilateral lower limb swilling
 Compartment syndrome  pain in calf Msc , May missed with
DVT,(which caused by stasis)& its treated with anticoagulants.
But treatment of Baker’s cyst is aspiration.

If the ptn comes with baker’s cyst , and

you give him a warfarin as a case of DVT ,
that increasing risk of bleeding caused by
rupture cyst  accumulate at post
compartment  pressure on Msc 
compartment synd  Msc necrosis &
amputation .

To differentiate between DVT & Baker’s cyst 

By Duplex Doppler

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Dr, Abdulraouf Abdullatif

2): Extra Arthicular: Less common presentation.

a) Skin Manifestations: most common, around 25% of cases related

1) subcutaneous nodule.
In remitting case and active
disease a nodule will
Rh- factor Antibody is appears, but if a disease is
ABs ,
responsible for nodule subcutaneous relapsing will disappear.
attacks
forming, so if found a
nodule  Rh-factor +ve (Nodule) ‫كل ماٌزٌد االلتهاب ٌزٌد حجم‬

Nodules indicate: mass

initiate inflamatory
formation process ,
(Nodule)
1/ active disease.

2/ severity by size. + Fibroblasts

,deposition of
fibers tissue .

Most common sites: 1/Extensor surface of elbow (single) & hand(multiple).

2/ wrist, sacrum & tendon Achilles.

*Nodule does not always visible, can get it by sensation (manipulation & palpation)

3/ sclera blurred vision  Ix, by fundoscopy & slit lamp.

4/Heart: myocardium fibrous tissue of formation  separation heart fibers 

no contraction  COP  H.F.

5/ lung  Asymptomatic.

*To differentiate nodule and bony protrusion by mobility, if movable  nodule

, if not  bone

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Dr, Abdulraouf Abdullatif

2) Palmer erythema:  Red as a reflex of V.D

vasculities at B.V of periphery of hand  Thickness  narrowing of

lumen  B.S to digits (ischemia)  pallor cyanotic

 3 Reynaud’s phenomena, its symptoms (parasthesia & tingling) 

treated by warming fingers (‫)دفٌهم‬,

If vasculitis incessant (permanent) even by warming, doesn’t reflex to

V.D  necrosis of digits 4 pyodermal gangrenosum & may +/- splinter
hemorrhage (rarely).

Abs attacks a Retinaculum sheat around the tendon of 4th& 5th 

fibrosis  attraction of fingers  5 Dubytrene contracture
D\D: liver cirrhosis, R.A, Alcoholics, epilepsy, phenytoin tox & vibrating tools.
Rx: by fasciotomy.

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Dr, Abdulraouf Abdullatif

b) Neurological manifestation :
1) Carpal Tunnel Syndrome: due to compression on Median nerve at
tunnel duct, the ptn complains of parasthesia & tingling of thumb,
index, middle & ½ ring fingers, usually at night resulting by
pressure on hand.
How to confirm?

*prayer test

*Phalen’s test:

*Tinel test: tab at groove

*Or confirm carpal

tunnel syndrome,
by:

Nerve conducting
study.

Causes of carpal tunnel syndrome:

Female (Grandma), Obese, old age, has h\o of D.M, and carrying her

ARM PIT up

A: Acromegally & Amyloidosis. P: Pregnancy.

R: Rheumatoid Arthritis. I: Idiopathic.

M: Myxodema (thyroid disease). T: Traumatic.

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Dr, Abdulraouf Abdullatif

2) Tarsal compartment syndrome :

In lower limbs (foot) complains of tingling & parasthesia.
3) Cervical cord compression : Atlanto Axial Sublaxation
 Tingling & parasthesia of upper limb.
4) Mono neuritis multiplex :one group of nerve affected (motor or sensory)

c) Ocular Manifestation :
1) Scleritis: most serious presentation painful and affect the vision & corneal erosion.
2) Episcleritis: not affect the vision & usually painless.
3) Kerato conjunctivitis sicca (Sjogran Syndrome ) dry eye ,
As foreign body sensation, it’s most common presentation.
4) Scleromalascia perforans :

d) Pulmonary manifestation:
*subcutaneous nodule which affect the lung  asymptomatic
 (1 caplan syndrome), Need to CXR to show it only.

* Abs attacks interstitium of lung (2 cryptogenic fibrosing alveolitis)

*Inflammation of pleura (3 Pleurisy)  pleuratic chest pain and Rarely pleural effusion.

e) Cardiac Manifestation:

rheumatoid nodule formed inside fibers of heart & contractility  H.F. Nodules
may compress the conducting system  Arrhythmia. Compression on Coronary
Artery  IHD by Vasculitis .
Inflammation of heart: Endo & Myocardium are V.Rare
Pericardium: common in R.A  pericarditis not ass’ with pericardial effusion

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Dr, Abdulraouf Abdullatif

f) Renal Manifestation:
R.A affects  Bowman’s capsule (basement membrane) which responsible
for protein filtration  appears a protein in urine (protein urea) 
Nephrotic Syndrome
Causes of Nephrotic Syndrome:
Direct: Amyloidosis  deposited in kidneys  erosion of Bowman’s capsule.

Not used
Indirect: Drugs therapy as Depencillamine & Gold Salts. now days

g) Musculoskeletal Manifestation :
Msc wasting, Myositis, tendinitis & Baker’s cyst.
Abs  e’ active disease  Generalized fatigability.

h) Lymphatic Manifestations :

Spleen lately affected after 15-20yrs of ptn with R.A

Chronic erosion of spleen  autoimmune disease  splenomegally &

hypersplenism  pancytopenia
Felty Syndrome: female, old age >50yrs, Caucasian,
WBC  NEUTROPENIA. long standing (chronic) Rh.factor +ve & rheumatoid
nodule.
RBC  Anemia
C\P: splenomegally + pancyopenia +R.A
PLT  thrombocytopenia Lyphadenopathy, wt loss, Kerato conjunctivitis sicca-
(dry eye) , chronic ulcers, skin pigmentation &
recurrent infections.

INV: Lab: pancytopenia + LFT abnormality &

impaired T &B Cell,(High risk to B &T cell Lymphoma

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Dr, Abdulraouf Abdullatif

i) Hematological Manifestation :
Commonly R.A Ass’ with Anemia, which caused by,
1) Chronic disorder.
2) NSAIDS long standing use  (Peptic ulcer & iron Def Anemia) .
3) Pancytopenia.
4) Megaloplastic Anemia, by Methotrexate action on Folic Acid as
antifolate factor, which decrease its absorption in duodenum and
jejunum.
5) Anemia b\c of Hypersplenism.

Investigation:

CBC: HB, WBC or (Felty Synd).

ESR & CRP:

LAB

Specific
X-ray: hand deformity.
ABs Imaging Nerve Conduction study: carpal tunnel.
Rh .f sero +ve
C.T: to exclude Atlanto Axial subluxation.
CCP
Slit lamp & fundoscopy  eye manifestation

Echo & ECG:  IHD, Arrhythmia, H.F

Abd U\S: splenomegally & hepatomegally.

14Urine Analysis: Nephrotic Syn.
 RH.F, Never ever back to
Dr, Abdulraouf Abdullatif normal in case of R.A.

1/ Rheumatoid factor: Relapse Remission

- IgM ABs AGAINST bodys IgG Abs. D\D of RH.F Sero +ve, 
- +ve, indicate Severity of the disease not Activity. 1/chronic infections.
- Sensitive 70-80% & not specific B\C of D\D 2/infective endocarditis.
3/Interstium lung disease.
2/Cyclic Cetrullated Peptide:
4/T.B.
Attack ‫كل ما‬ 5/hypogamaglobulinemia.
,‫بتزٌد‬ 6/scleroderma.
- Highly specific & not sensitive.
CCP ً‫بٌكون عال‬ 7/ Sjogran Syndrome.
- 30% of ptn with R.A. 8/ people exposed to
-Can find also in recurrent sever cases (acute stage). radiation.

3/ Anti Nuclear Abs:

- Highly sensitive & not specific.

- All cases of Rh.F +ve.

Radiological Feature of Hand:

 Soft tissue Swilling.

 Periosteal osteopenia Ca+.
 No Arthicular Space.
 Deformity.
 Ulnar Deviation.
 Ankylosis (arthicular spaces
fusion)

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Dr, Abdulraouf Abdullatif

EX:

Plain x ray showing P\A

View of hand with:

1
4
1/ Ankylosis. 2/ Z deformity.
2 5
3/ soft tissue swilling. 3

4/ periosteal osteopenia.

5/ ulnar deviation.

*** Specific Criteria: 4/7 confirm the diagnosis.

By H\O, 1) Morning stiffness than 1 hr lasts for or > 6 wks.

By Ex, 2) polyarthritis than 3 joints affected.

If you get a CCP +ve
3) Small joints > large joints. confirm a R.A even
without Criteria.
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Dr, Abdulraouf Abdullatif

4) Symmetrical.

5) Subcutaneous nodule.

By INV, 6) Rh.F  Sero +ve.

7) Evidence of radiological changes of X-ray.

Management of Rheumatoid Arthritis:

The important note, that we should know, a treatment for R.A (CANT BE AS A SINGLE
TREATMENT)  TEAM WORK TREATMENT.

- Orthopedics to treat deformities.

- Occupational. – Psychotherapy  depression (group therapy).
- Physiotherapy  rehabilitation.

Medical Therapy:

1) Rest during active disease. b\c movement inflammation.

2) The only drugs that decreased a progression and inflammation
is DMARD (Disease Modifying Anti Rheumatoid Drugs)DOC
1/ PROGRESSION.
Aim
2/ DISABILITY.

3/ IMPROVE OUTCOME.

4/ preserve function.

Need 8-12 wks to be effective, so should reassure the patient

about drug action & add a NSAIDS to reduce the pain, but
avoided in Patient with GIT erosions (Peptic Ulcer) by history
taking.
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Dr, Abdulraouf Abdullatif

If not responded to NSAIDS Add High dose of steroids for8-12wks,

Its S\E is Cushing Syndrome; reduced it by adding Steroidal Sparing

Drugs  (Azathioprine & Cyclosporine) with Steroid Low Dose.

The all are mentioned above are not effect on the course of the disease,
but to decrease a pain.

DMARD’s: ‫نستخدم واحد منهم‬

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.

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: fibroblast  pyodermal gangrenosum & S\C Nodule.
So it’s the best for s\c manifestation.
4/ Gold salts :
5/Depenicillamine : Not given Now Days B\C Nephrotic Syndrome..
Thrompocyopenia.
Leukopenia .

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Dr, Abdulraouf Abdullatif

*** Tissue Necrotizing Factor (TNF) modulator agent :

1/ Inflximab(immunosupprasent):CD20 Inhibitor  for the last stages in resistance cases on
methotrexate .
2/Anti TNF: ‫كان المرٌض فات فٌه و خدي‬
‫علٌه مش حٌأثر فٌه اي عالج‬
*** IL1 antagonist  anakinara .
. ‫تانً م غٌره‬

Poor Prognosis:
1/ Age of presentation if than 60s yrs.
2/ Sudden Onset of multi systemic involvement.
3/ symptoms lasting for more than 12 months.
4/ if primary presentation is an extra arthicular.
5/ early deformity within first 6 months.
6/ Anti CCP b\c Appears mostly at recurrent severe attacks.

2) Systemic Lupus Erythromatosis (SLE)

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Dr, Abdulraouf Abdullatif

Def: chronic relapsing and remitting polyarthicular disease which lead to

multi systemic involvement, due to circulating immune complex and auto
anti bodies.

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 b\c appears
at any sero +ve

2) Double strander DNA Abs 50%of cases  highly specific & Low sensitive, +ve in recurrent
severe SLE cases.

3) Rh.F  low sensitivity & specificity.

4) Anti RO & Anti LA: related with pregnancy,

Pregnant female with SLE 
-ve Anti RO & LA no effect on fetus, so can get pregnant.
+ve Anti RO &LA (transferring by placenta).  Infertility. Or  Spontaneous Abortion.
Or  Intra uterine fetal death. Or  Neonatal Lupus  Congenital Heart Defect 3th degree
Heart Block.
N.T: Avoided by screening before pregnancy.

It’s propagated by sunlight.

B) Environmental:
Exacerbated by estrogen & progesterone.
C) Hormonal:

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Dr, Abdulraouf Abdullatif

***Clinical Picture***

1\ Arthicular

2\ Extra Arthicular: which the most common presentation,

80% mostly with skin manifestation.

1) Arthicular:

-polyarthicular affects large joints than small joints.

- Asymmetrical.

- Migratory (flitting) or (fulminate), so it’s reversible after affection,

Previous H\O of joint pain & then back to normal affect other joint.

-Non erosion, Non destruction of joint.

-Deformity  resulting by tendonitis  Rupture of tendon  Deformity

Which Called (Jaccauds arthropathy) deformity resulting by tendonitis

It can be feature
In SLE, Have no specific Character.
of disease.
-Pain, tenderness, swilling & Redness.

How do detect 2ry Infection in SLE  D\D of Malar Rash:

By CRP, becauz its normal unless patient  infection . 1\SLE. 2\ mitral stenosis.

2) Extra Arthicular: 3\Emphysema (α anti trypsin Def).

4\cushing Syn . 5\ Rosacea.

a) Skin manifestation: is the most common feature of SLE.
6\ Hypo thyrodism. 7\ physiology.
1\ Malar Flush (Butter Fly):
8\ shines ‫مش كاترة‬
- Painful & itchy. - Affect Nose & Cheeks, & Sparing of Nasolabial fold.

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Dr, Abdulraouf Abdullatif

2\ Alopecia:
- Non scaring Alopecia, at remitting stage hair grows and at acute stage hair fall.
(Reversible).
- Discoid Lupus :red plagues with crusts
Arm  most common in extremities.
Scalp  scarring alopecia by fibrous tissue growing.

3\ photosensitivity:

Common in Africans (black) When exposed to sun light  Will increasing manifestation.

Rx: by sun blocking creams.

4\ Mouth Ulcer:

Early painless but if exposed to infection lately painful.

5\Nail fold Infarction:

Peri angular erythema due to of vaculities & ass’ with Splinter Hge (common).

6\ Reynaud’s phenomena :

Pallor  bluish  redness,

Relieving by warming if constant  CA+ channel blocker

(Nefidapine).V.D

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Dr, Abdulraouf Abdullatif

7\ Levedo Reticularis:
Redness + patchy pallor colure of skin (Arms & L.L).

B) Neurological Manifestation:
1\ Psychosis ,‫ ٌتخاٌل فً اشٌاء‬affect visual & auditory
function.

2\ Electricity affection by Abs and reduce transmission  Epilepsy.

3\ Peripheral Neuropathy, less common.

C) Lung: Pleursy  ILD .

D\ Cardiac:
Endo Myo  pericarditis  Pancarditis (Non infective) (LIBMAN SACKS SYN)

E\ Renal:
Vasculitis  B.V of Bowman’s capsule 

Nephritic Syn [Haematuria & Proteinuria] .

Mechanism:

Vasculitis of B.V  Edema compression  B.F to kidney  GFR

+++ JGA (juxta glomerular apparatus)  Renine

Angiotensinogen AgI Lung

Angiotensin converting Enz

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Dr, Abdulraouf Abdullatif

UTI Oliguria B.P V.C AgII

Mimics renal colicky pain ‫شبٌه بمغص الكلى‬

Salt & water retention

F) GIT Manifestations:
Severe Abd pain (epigastric)

*Abs  peritoneum  peritonitis. *Increase risk of peptic ulcer.

*Ampulla of vatar (edema)  Acute Pancreatitis

G) Hematology:
Autoimmune hemolytic Anemia. (Most common). INV: by Coombs test 
adding of Agglutinin to blood of pts With autoimmune disease  +ve clotting of blood
(So there is Abs in blood).

N.T: Lymphadenopathy common 50% LAB

Splenomegaly 20-30%
CBC: H.B *Anemia (Auto immune
Investigations of SLE Hemolytic Anemia).

Comb’s test  +ve.

LAB
*Pancytopeniasplenomegally.

ESR increased & CRP (normal) if indicate

Specific infection.
Abs DS Imaging RFT: high risk of mortality rate b\c of
hypertension, by renal involvement,

So DOC is ACE inhibitor B.P

Proteinuria

*Renal biopsy  glomeulonephritis, to use

high dose steroid  to decrease progression
24 of End organ damage.
Dr, Abdulraouf Abdullatif

ABs

ANA: 90% +ve, high sensitive & low Imaging

specific.
X-ray of affected joint: slight erosion,
Ds DNA Ab: highly specific.
B\C SLE its non destructive.
Anti RO & LA: Pregnancy.
EEG: for neurological manifestation.
VDRL: Venereal Disease Research
Laboratory, Specific for Syphilis Abs CXR: lung (ILD).
may result here as false +ve, by cross ECG &ECHO: for Arrhythmia, H.F &
reaction which is interacted with its pericarditis.
similar Abs.
Endoscopy: *Peptic ulcer.

Diagnostic Criteria for SLE: *** Clinically (Mostly)

* Skin manifestation 1) Mallor Rash. 2) Discoid Lupus. 3) Oral ulcer.

4) Photosensitivity. 5) Arthritis (than 2 joints)

* 6) Serositis; inflammation of any serous fluid of the body # Peritonitis. # Pleuritis.
# pericarditis.

7) Renal involvement <even with slightly proeinuria>.

*8) Hematological Disorder: whatever the type of Anemia.

*9) Neurological Disorders: Epilepsy.

*10) By INV: *Immunologically: ANA & Ds.DNA.

If more than 4 makes Diagnosis most likely, But confirmed by +ve (VDRL & Ds.DNA).

N.T: *May initially presented with Arthicular manifestations  overlapping,& years later
show a skin manifestation  Atypical SLE.

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Dr, Abdulraouf Abdullatif

Management of SLE:
The important note, that we should know, a treatment of SLE (can’t be as single treatment, team
work treatment)

- Occupational. – Psychotherapy  depression (group therapy).

- Physiotherapy  rehabilitation.
- Orthopedics to treat deformities (not mostly)
- Education of Patient about the disease relation with, Sunrise  sun blocking creams.
*pregnancy  screening of Abs.

*Coetaneous: DOC is anti malarial drugs (Hydroxychloroquine & Dapson creams) If not
responded,  Methotrexate cream (strong immunosuppressant).

*Joint manifestations: Hydroxycloroquine but if not responded  NSAIDS,

Joint manifestations, polyarthicular, large joints, asymmetrical, Migratory, swilling & redness  the
same manifestations of Rheumatic fever , so can be differentiate by Drug response , give
Hydroxychloroquine or NSAIDs if  dramatically response within 24hrs R.F ,if take weeks or
months its SLE .

*reynauds phenomena: Ca+ channel blocker (Nefidipine)

*End Organ Damage : visual hallucination, tonic clonic convulsions, renal involvement, cardiac
involvement  immediately Start with High Dose Steroids (I.V, Orally , Topical) .
Long term treatment of steroids  Cushing Synd  Give Steroidal Sparing Drugs (Azothioprine
& Cyclosporine).

*If Develop case to Hypertension, DOC is ACE inhibitor (captopril).

*Life span of SLE cases is depending on End Organ Damage, usually 90% of them
Life span exceeds 5yrs survival rate.

26
Dr, Abdulraouf Abdullatif

N.T* Some people has genetic predisposition (Anti phospholipids Syndrome) by

used 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.

*causes of Death in SLE:

1/Renal Lupus nephritis. (Mostly)
2/CNS Involvement.
Drugs induced symptoms:
3/Cardiac IHD,
1/Aspirin high dose 300mg long a) Vasculitis.
2/ Phonation , 3/ methyl dopa .
b) S\E of steroids by [atherosclerosis,
4/ phenobarbitone. 5/ isoniazide
6/procaine amide. 7/ hydralazin.
polycythemia & +ve inotropic 
8/ Minocycline. 9/ B-Blocker. [( force contraction), or infection b\c long
use of steroids].

3) Scleroderma (progressive Systemic Sclerosis )

*Def: Chronic Multi systemic Involvement with unknown etiology, which affects
micro blood vessels & Skin.
*Autoimmne: -female 4:1. – Middle aged group. -+ve F\H.
– ass’ with other autoimmune diseases.
– Antibodies (Rh.F, ANA, ASD70 & ACM Abs)  skin & micro vascular disorder.

Skin Micro vascular

Onset : *initiates later on. *Initiates firstly before Skin
manifestations.
Mechanism *Autoimmune inflammation *Vasculitis  narrowing of B.V
: invasion of skin by T  Ischemia ( end organs &
Lymphocyte +Fibroblast  periphery of digits)
deposition of collagen & fibrous
tissue  thick skin and
tightened (shiny skin) no skin

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Dr, Abdulraouf Abdullatif

turgor.
C\P: 1/ mostly deposition of fibers in 1/Years with no complains except
Face  Mask Face, b\c of , Reynaud’s phenomena
thickening . 2/May ass with edema  sausage
2/ by stretching  tapered like fingers (as acromegally)
Nose. 3/ Inf  ischemia  necrosis
3/ Microstomia (Fish Mouth) . of tips of fingers with
4/ hyper pigmented with hypo fibrous tissue  long & tapered
pigmented areas, b\c atrophy of fingers Sclerodactyly,
some melanocytes, called
D\D: D.M, T.B, ‫صوابع طوال ورقاق‬
Salt & pepper appearance.
vibratory tools.
4/Continued Ischemia necrosis
White people hyper pigmentation
 Amputation (indicates
Black people  Hypo pigmentation. chronosity).

Other Manifestations:

1) Joints: non erosive mild arthritis at beginning, then in severe case  Erosive
Arthritis deformity (no specific character).

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Dr, Abdulraouf Abdullatif

2) GIT: *Esophagus: fibrosis of wall no Peristaltic movement  Dysphasia.

Fibrosis at cardiac sphincter  GERD.
*Stomach: fibrosis  small in size  Early Satiety. D\D Gasrtric outlet obs:
1\Scleroderma.
* Duodenum: fibrosis pyloric stenosis 
2\ Duodenal Ulcer.
Gastric outlet Obs  Projectile vomiting.
*Intestine: fibrous tissue  villi atrophy no movement of bowel 
Bacterial overgrowth  Malabsorption (Blind Loop Syn)  Diarrhea
cachexic  Statorrhea.
3) Pulmonaryass’ with ASD70 Abs : ILD  erosion of micro vascular of lung
 Pulmonary Hypertension  R.t Side H.F (Cor pulmunale) cause of Death.
4) Renal Involvement: erosion of B.V  Glomerulonephritis  Nephritic Syn
Hypertension crisis cause (Death).

*Types of Scleroderma:
Limited Scleroderma : Diffuse Scleroderma :
Coetaneous manifestation mainly Coetaneous manifestation mainly
affects face, Hands & feet distally, affects large area of skin with
with no end organ damage, CRESTSyn internal organs & presentation of
C: Calcinosis. CREST Syn .
R: Raynauds Phenomena. *ASD70 Abs.
E: Esophageal Involvement. * Poor prognosis.
S: Sclerodacytly.
T: Telangectasia.
*+ AC Abs .
*has good prognosis.

29
 CBC: Anemia of chronic illness WBC.
Dr, Abdulraouf Abdullatif ESR & CRP normal unless in case of
infection mostly gastroenteritis.
* Investigations of Scleroderma: LAB RFT: Renal involvement.

ASD70 (Diffuse type) Specific

& AC Abs (Limited Type), Barium Meal: Esophagus.
to confirm Dx. Abs Imaging Barium Enema: Intestinal
Manifestation .
No specific criteria,
Skin biopsy in
untreated case.
‫مدخل لالسئلة عند‬
ً‫دكاترة الطب‬
Management: symptomatic therapy. ‫والخضرا‬

1) Skin Manifestation  Methotrexate or Dapson.

D\D of thick Skin:
2) Blind Loop Syn Abc’s. 1\ f\h. 2\ Acromegally.
3) Lung  High dose steroids. 3\ scleroderma. 4\ D.M chronisty.
5\Corrosive vapor.
4) Kidney  ACE I  B.P.
5) Arthritis  NSAIDS.
6) GERD  omeprazole (proton pump inhibitor).
7) Gastric Outlet Synd  Surgery.
Poor prognostic factor:

 5years survival rate.  Up to 70%. -Old age. -Pulmonary HTN.

-Proteinuria. - ESR
- Diffuse skin disease.

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Dr, Abdulraouf Abdullatif

5)Sjogrens Syndrome
Def: Autoimmune disorder affects exocrine glands, which is filled with
T-lymphocytes & fibroblasts  damage of glands:
Autoimmune:
*submandibular (salivary glands).
- female 9:1. - Middle age.
*Lacrimal glands. -+F\H. -HLA B8&Dr3
*Vaginal glands. - ass’ with autoimmune dis.
*Myasthenia grave’s. -autoimmune circulating AB:
*Chronic Hepatitis.
(Rh.F, ANA, Anti RO&LA).
*R.A * SLE. *KCS.
*1ry biliary cirrhosis.
Damage of,

*Salivary Glands  Xerostomia (dry mouth), so no (chewing, speech & swallow).

*Lacrimal Glands  Xerphtlamia (dry eye)  F.B sensation, itching & redness.
*Vaginal Glands  Dyspareunia (painful sexual intercourse), Decrease its secretions  highly
risky to infection.
* Parotid Gland  Enlargement b\c of fibrous tissue deposition  parotids.

Other features,
*non erosive Arthritis. * Reynaud’s phenomena. * Fever, myalgia, arthralgia

*lymphadenopathy  40 times more risk for lymphoma.

Investigations:

1/Saxon test  reducible test of xerostomia, by chewing on folded sterile sponge for 2 min. ‫تقٌس‬
‫وزن القطن المستخدم تلقاه مازادش‬

2/Schemer test  to Xerophthalmia. .‫باستخدام ورقة خاصة وتوزنها‬

3/Anti RO 70%, Anti LA 30%. RF(90%) & ANA(70%)

4/buccal mucusa biopsy

Management: 1/ dry eye, artificial tear or dark glasses.

2/dry mouth  pillocarpine. 3/ vaginal lubrication creams

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Dr, Abdulraouf Abdullatif

6)polymyositis & Dermatomiositis

Polymiositis: Inflammation of Skeletal Muscle

Dermatomiositis: Inflammation of skeletal Muscle & Skin Involvement.

*Etiology is unknown but mostly, autoimmune  Autoimmune: 1- female 3:1. 2- Middle

*Incidence  2-10 /1000, 000. age. 3-+F\H. 4-HLA
Dr3 5- ass’ with other Aut
I Dz 6-autoimmune
circulating AB: (Rh.F, ANA, Anti JO1).
Path physiology: Autoimmune Destruction of Muscle Mostly  Skin manifestation. *mostly
inflammation affects Bulky Msc which is a proximal Msc’s.

Character: b\c of systemic involvement atrophy of Msc  symmetrical Msc weakness (painless) at
beginning  then (painful)  Myalgia & Arthralgia.

C\P: mostly presentation of Both by skeletal Ms involvement , painless Ms weakness early which characterized
by symmetrical ( bilateral ) of proximal Msc’s ( Distally Proximal ) Lower limb then  Upper limb of proximal
Ms  Myalgia & Arthralgia .

D\D: *Guillain Barre Syndrome. ‫ البداٌة مانقدرش نقعمز كوٌس‬: ‫سٌنارٌو الحالة‬
*Toxoplasmosis. ً‫مانقدرش نركب الدروج ومانقدرش نمش‬
. ‫بعدٌن مانقدرش حتى نمشط شعري‬
Other Muscle affected:
1\ Diaphragm  Res Failure (Apnea) admitted  M.V & I.V Steroids & observed may need to
intubation.
2\Esophagus  Dysphgia.
3\ Larynx  Horsens of voice (V.C)  admitted  laryngeal spasm & need I.V steroid &
observation may need intubation.

32
Dr, Abdulraouf Abdullatif ‫لبس الهنود‬

*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
 called Gottoren sign with mechanical Rash .‫احمرار عالمفاصل فقط مع حكة‬
5\ Calcinosis cutis thickening of finger tips.

6\Reynaud’s phenomena. 7\Joint Swelling (large joints) not common.

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 *CBC, ESR &CRP  .
Dr, Abdulraouf Abdullatif * Msc Enzymes: 1\Creatnine Kinase 
severity only, in 70% of cases.
Investigations : LAB 2\ Lactic Dehydrogenase  the same, both
used as screening marker.
Rh.F+ve, ANA +ve, & *Urine analysis (Myoglobin) 
Anti JO1AB  +ve, not myoglobinuria +ve  severity & activity of
sensitive. So its absence disease.
doesn’t exclude a disease. Specific

Abs Imaging

Msc Biopsy  projections of T.Lymphocytes & *Electromyogram (EMG), to distinguish

fibroblasts. The best diagnostic goal Standard from neurological disease. (G.B.S
to confirm,may it does not confirmatory &Toxoplasmosis).
100%, May presented as patchy type  -ve
Msc biopsy & it does not exclude the disease,
so need (MRI guided biopsy) from fibrotic
muscle, to show patchy type.

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

1\ High dose of steroids orally, except in cases with Diaphragm involvement & Laryngeal spasm
given I.V.
2\ Dyspnea  Mechanical Ventilator.
3\ Myopathy resulting by a treatment side effect  ptn presenting by weakness without skin
manifestations and he was known as case of dermatomyositis  reduce the dose of steroid and
adding of [methotrexate or azathioprine] to preserve the remission stage.

Prognosis: if not starts with steroid pts may die by Respiratory apnea, so should start
immediately with high dose steroids good prognosis.
Necrotic tissue may change to malignancy in people who older than 60yrs.

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Dr, Abdulraouf Abdullatif

*Sero –ve group: HLA B27

1)Ankylosing Spondylitis : its chronic slowly progressive arthritis which mostly

affecting Sacro-iliac joint . - affects male > female 3:1

C\P: SOCRAT Site: lower back pain (sacro-iliac j).

Severity: sever early morning pain.
H\O:
Onset: gradually.
1\loss of lordosis. ‫مشٌت الدٌك‬ Character: electrical dull pain.
2\ range of spine movement. Radiation: ascending to spine & Gluteal region.
3\ decreased chest expansion. Relived: by movement.
Aggravating: Coldness.
Ix:
Associated: 1\ 2ry osteoporosis. 2\ spinal #.
Pelvic U\S: prostatic enlargement 3\peripheral arthritis. 4\ Ant Uveits.
ECG: Pericarditis&conducting 5\Prostatits 80%. 6\ pericarditis.
defect bradycardia 7\M.R & A.R. 8\ amyloidosis. 9\ pulmonary fibrosis
Echo: MR&AR. Timing: early morning.
Fundoscopy: Ant uveitis.
Dexa Bone scan: osteoporosis.
CXR: pulmonary fibrosis.
C.T of Spine: loss of normal lordosis
on lateral view & vertebrae cubes
called bamboo stick spine.

Rx: Reassurance
1) swimming to asses back Muscles.
2) Lower back pain  NSAIDS.
3) Peripheral arthritis & end organ damage
 DMARDS (Methtrexate& sulfasalasine).
4) Modification of life by feature.

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Dr, Abdulraouf Abdullatif

2) Reiter Syndrome : (Reactive Arthritis ) :

*if pts complaing of symmetrical arthritis (only joint) reactive arthritis.

*asymmetrical arthritis. *Urethritis. *Conjunctivitis Reiter Synd

*Male > female 15:1, (20-30 years)

Triggered by infections usually infectious Diarrhea caused by food poising

(salmonella dysentery),

Differ from person to person b\c of triggering factors (genetic predisposition).

C\P: *patient can’t see cant pee, can’t climb a tree.

* Male genitalia, may affected which cause  circinate balanitis (ulcers on male
organ) [missed with syphilis, Behcets or any infectious disease]
*Keratoderma blennorrhagia: .‫قشور صفرا من ااسفل الرجل وكانها التهاب فطري‬
*Oral ulcer (painless) geographical tongue. ‫ماتجٌبش سٌرتهم قدام‬
*Nail Dystrophy. . ‫الدكتور اال لو سئل‬

*Rare Complications:
Heart  Aortic incompetence, conduction defect.
CNS  Convulsion & peripheral neuropathy & meningoencephalitis.

Investigations < the best is History & proved Examination >

Rx: use Steroids  responded to most of cases& resolute, used until disappearance
of symptoms.

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Dr, Abdulraouf Abdullatif

D\D of monoarthicular synovitis: mono arthralgia .

1\Sepsis (septic arthritis) .

Crystal Induced Arthropathy: 2\ trauma (direct or indirect [twisting injury] ) .
3\osteoarthritis.
4\hemarthrosis (hypercoagulable or drugs [warfarin]).
5\R.A &SLE (initially mono then polyarthicular)
6\ Gout or Pseudogout.
7\ juvenile idiopathic mono arthicular.(pediatric)

Gout Pseudo Gout

Mono articular synovitis due to Mono articular synovitis due to
deposition of mono sodium urate mono deposition of Calcium pyrophosphate Di
hydrate crystals (MSUM), derived hydrate (CPPD) Crystals.
from uric acid most likely. So if its
normal does not exclude the Dx b\c it
may produced by other sources. Mostly with female.
*Mostly with male.
Same
The uric acid increasing by:
1\ production :
*endogenous: purine turn over
(cell lyses ) as in *Ch Myeloid Leukemia
 WBC which rich by uric acid 
rupture (tumor lyses syndrome ) &
escape of uric acid & Polycythemia RBC .
*exogenous: digestion (meat)
2\ excretion (renal tubule defect) most
common.
*congenital: isolated RTD. (Pediatric).
* Renal failure.
*Drugs: - Loop Diuretics & (Thiazide.)
– Pyrazinamide. -Cyclosporine. – lead
– Low dose Aspirin b\c long standing use
- Alcohol (lactic acidosis).

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Dr, Abdulraouf Abdullatif

*Acute symptomatic Gout: MSUM

Arthritis: crystals deposited at *Acute symptomatic Pseudo Gout :
1stmetatarsal phalngeal joint (big toe) Arthritis: red hot tender swollen joint
 hot, swollen & tender (podagra).  mainly affect Knee joint but may also,
Other joints: Ankle, Knee, wrest & wrist & Shoulder.
Elbow. Distinguished with gout, by
arthrocentesis  type of crystals.
*Chronic Gout:
- Arthralgia: very severe in sudden *chronic pseudo gout :
manipulation painful. - Arthritis: chronic joint pain.  b\c
–deposition to other sites : 2ry osteoarthritis  arthro plasty.
- white nodules formation  rupture 
release MSUM(2ry infection )  Tophy
 skin of extensor surfaces of Wrist,
Elbow, fingers, Achilles tendon , ear
auricle .
-deposited in kidney  Renal Failure

Gout

Investigation:

Arthrocentesis (aspiration): it’s *CBC:  WBC.

diagnostic *ESR (Severity) &
*Spindle shaped  Na Urate. LAB CRP (Prognosis)  screening
* Cuboidal  Ca pyroph

Specific
X-ray punch out lesion.
Abs Imaging

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Dr, Abdulraouf Abdullatif

Management:

Pain  NSAIDS (Endomethacine) analgesia & anti inflammatory. For both.

If not responded to NSAIDS  steroid cream,

not res  colchicines tab (anti inflammatory) in acute stages,

N.B : but never ever use in acute stage  Allopuranol (acute inflammatory rxn) .

If not responded to cochicines oral or Inta articular Inj of steroid.

After management of acute, Send Biopsy of arthrocentesis to distinguish

between both, Gout or Pseudo Gout if gout  allopuranol as prophylactic.
If pseudo gout  decrease causes of it (osteoarthritis) 
w.t, analgesia (endomethacine & paracetamol)  Arthroplasty. Does not give
Allopuranol b\c have no effect on Ca pyroph
crystals.
Allopuranol: hypo uracemic agent.
*used in:

1-recurrent attacks, not in acute attacks.

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
39
Dr, Abdulraouf Abdullatif

Behcets Disease:

*Def: Multi systemic vasculitis of unknown etiology, affecting arteries & veins,
common in male than female, (20yrs -40yrs) .
*it’s not autoimmune but related with HLA B51.
B\C:1\ male > female. 2\ not ass’ with other AID. 3\ No specific Abs. 4\no FH
pathophisiology:
*Irritation of blood vessels  edema  compression (narrowing) of B.V ischemia of artery &
later on necrosis  weakness of vein wall  aneurism.

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 (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
(hyper sensitivity)
due to mechanical stimuli  pustule formation.
By sterile needle  stick 
at local site (make sign) then chick the site
 induration (redness hotness & rash)

*Dx, clinically:

2minor criteria +major Behcets disease.

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Dr, Abdulraouf Abdullatif

Main Presentation: recurrent oral ulcer

Recurrent genital ulcer Uveitis (ant mostly)

Other manifestations:
1\ Abdominal Pain & diarrhea  vasculitis of SMV of intestine b\c Malabsorption.

2\ Headache  b\c of non infective meningitis (aseptic) escaping of inf mediators in circulation
affect on meninges.

3\ venous system  DVT  aneurism.

4\ Arthritis (inflammation B.V of joints  arthritis self limiting) non destructive

Management:
*Steroid (topical or orally)  inflammation.
*Chalichicine  joint involvement.
* Immunosuppressant.
*Anti fungal  ulcers 2ry infection.

Vasculitis of Artery only:

-Large Blood Vessels  Aorta & its main branches.

–Medium B.V  branches which supplies organs.
– Small B.V  terminal.
A synchronized pulse.
Large B.V: Small B.V:
1\Giant Cell Arthritis. 1\wegners granulomatosis.
2\ Takayasu’s arthritis:uni latral inf of large b.v . 2\ microscopic polyangitis.
3\ churg-straus’s syndrome.
Medium B.V:
4\ henoch schneil purpura.
1\classical poly arthritis nodosa.
5\Mixed essential erythroglobulinemia.
2\Kawasaki disease.

41
Dr, Abdulraouf Abdullatif

*Giant cell arterits: arterits of large blood vessels (temporal & ophthalmic B.V).
*affects female older than 60 yrs.
C\P:*blurred vision, *temporal headache localized & *pulstile palpable temporal B.V *blindness 
is reversible if managed early, Or permanent if does not treated immediately.
Investigation: *Angiography  narrowing in B.V.
*Biopsy: most confirmatory test from Temporal a’  non caseating granuloma .

Treatment: give high dose of steroid immediately to prevent end organ damage & blindness .

Poly arthritis nodosa: (PAN)

Affects multiple medium sized blood vessels which supplies organ with skin manifestation .
Its autoimmune disease mostly affects male 2:1 aged more than 40yrs.
Affect males > female’s b\c Abs reaction to HBV which is incidence in male > female. Abs attacks
multi organs  destruction. Lead to inflammatory rxn inside the body (flue like symptoms).
1\skin: most common , nodules (pin point bruises & erythema ) & levedo reticularis
2\ 70 % affect vasa nervorum  neuropathy affects (motor & sensory) mostly symmetrical.
3\ Hypertension b\c of local vasculitis.
4\ renal involvement (glomerulonephritis) v.rare.

Investigation:

*Angiography OR Biopsy in (case of organ damage).

Management: High dose steroid, once start treatment the prognosis very good.
-50% relapsing  give steroid to remission stage. –
mortality rate < 20%.

Wegners granulomatosis: vasculitis of small blood vessels common in female mostly of (nostrils,
eyes & ears).

See page # 2

Thank you D.R Abdulraouf,for his good manners & creations

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