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 Rheumatology

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dr saad
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عدد المساهمات : 176
تاريخ التسجيل : 12/12/2010
العمر : 35
الموقع : http://medsurgery.ba7r.org

مُساهمةموضوع: Rheumatology   الجمعة 01 أبريل 2011, 20:47

Arthritis
1- Septic.
2- Osteoarthritis. (Wt. bearing knee, hips in elderly & obese).
3- Seronegative.
4- Seropositive  SLE, RA.
[1] Septic arthritis:
All monoarthritis is septic arthritis until proven other wise.
- Synovial NF > 50,000.
- Acute onset.
- With fever & chills.
- Positive culture.
- More commonly in knee.
[2] SERONEGATIVE:
1* Ankylosing spondylitis:  4 As:
- Apical lung fibrosis.
- Aortic regurge.
- Anterior uveitis.
- Achilles tendonitis.
HLA-B27
Spine – sacroiliac joints.
Pain on rest, improved on exercise.
Bamboo spine & Syndesmophyes (Tramline appearance) in an x-ray.
2* Reactive arthritis (Reiter's Syndrome):
1- STD.
2- non STD.
(urethritis, conjunctivitis, arthritis).
Rash:
Keratoderma blennorrhagica: on palm & sole.
-Circinate balanitis: on glans & prepuce.
3* Psoriatic arthritis:
- A symmetrical inflammatory oligoarthritis.
- Symmetrical polyarthritis: like RA.
- Predominant distal interphalangeal joint arthritis.
- Psoriatic spondylitis: like ankylosing spondylitis.
- Arthritis mutilans.
Extra articular:
Nail: onycholysis, pitting, sublingual hyperkeratosis, horizontal ridging.
Skin: scaling on extensor.
4* (Enteropathic Arthritis) Arthritis with inflammatory bowel disease
(IBD):
Ankylosing spondylitis & sacroiliitis with diarrhea.
5* Bachet syndrome:
Recurrent oral / genital ulcer.
Recurrent thrombi: CVA, DVT, optic.
6* Whipple's disease:
Arthritis + Hyperpigmentation + LN + Splenomegaly.
[3] Seropositive:
1- RA:
Significant morning stiffness or joint pain must be more than an hour.
INVESTIGATION:
1- Base line for all patients
2- Specific.
(1) BASE LINE INVETIGATION:
1- CBC  cytopenia.
2- ESR, CRP.
3- Urea & electrolyte  to assess kidneys.
4- LFT.
5- HBV, HCV  cryoglobulinemia.
6- Urine analysis (protein, hematuria, cast).
7- X-ray (chest).
8- ECG.
(2) SPECIFIC:
- ANA  SLE may be for the other also.
- Anti-ds DNA, anti-Sm Abs  SLE.
- RF  present in 70% of cases  RA.
- The most specific test for RA is anti-CCP Abs which is anti-cyclic citrullinated
peptide  positive > 95% (new & still not written in text books, a rheumatologist will require it).
- X-ray (hands, knee, feet, cervical atlantoaxial joint)  RA.
- Upper GI endoscopy,
- Motility test  scleroderma.
- Anti-Scl 70  Scleroderma.
- P-ANCA  if chest pain + hemoptysis / antiglomerular basement membrane
(anti-GBM).
- All patients with hematuria & proteinuria more than 1g  DO Renal Biopsy
regardless of renal function test.
- If u suspects complement  Do: C3, C4.
2- SLE:
Criteria to diagnose SLE;
Remember this word  SOAP Brain Md
Four out 11 is considered ok to diagnose SLE:
1- Butterfly molar rash cross the nasal bridge  doesn’t cross nasolabial fold
because if it does we’ve to think  hypothyroidism, polycythemia ….
Dr. Fatah Aldien said,, it could be found in the buccal mucosa and labia
majora.
Also doesn’t leave scar... and it’s erythematous.
2- Discoid rash  it’s raised erythematous found more commonly in the scalp
area… also leave scar.
3- Photo sensitivity means the redness increase when exposed to sun... or
new redness formed in exposed area.
4- Oral ulcer.
5- Arthritis  non erosive  small (peripheral) joints.
6- Serositis  pleura, pericardium.
7- Renal disorder  can be asked like this…any proteinuria (frothy bubbles
seen with the urine) or New Hypertension…or lower limb edema or any
edema.
8- Neurological disorder  seizure or psychosis not depression.
9- Hematological disorder:
A-Hemolytic anemia.
B-leucopenia less than 4000.
C- Lymphopenia less than 1500.
D- Thrombocytopenia less than 100.000.
10- Immunological disorder:
a- anti phospholipids' Abs.
b- anti-Ds DNA Abs.
c – anti-Sm. Abs.
d- False positive syphilis serology.
11- ANA positive > 95% of cases.
Let’s go through each system:
1- CNS: 60%.
-Convulsion and seizure.
-Psychosis  we’ve to know is it due to SLE or Cortisone treatment side effect? 
By:
-myopathy  due to cortisone side effect.
-depression and vasculitis  stroke.
2- eye:
(1) Anterior Uveitis but more with RA.
(2) Dry eye plus dried mouth  sjogren syndrome.
Schirmer's test  put litmus paper strip.
if it's wetted by tear  change the color.
 15 mm is normal.
(3) Cystoid bodies (on microscopy) / by ophthalmoscope  cotton wool spots.
(4) Subconjunctival hemorrhage.
3-Neck:
Thyroiditis.
4- lung:  Dr. Abeer Kawther:
1) Vasculitis  fibrosis, thrombosis (lung infarction).
2) Pleurisy.
3) Recurrent DVT  pulmonary embolism.
4) Pulmonary edema due to secondary HF.
5) Immunosuppression (immunity) by SLE or steroids (drugs)  prone to
infection  Tb or atypical infection.
6) Pneumonitis (non-bacterial, due to vasculitis)  like lobar pneumonia.
7) Pleural effusion  transudate.
Cool Shrunken lung syndrome  due to bilateral fibrosis (fibrosing alveolitis).
9) obliterative bronchiolitis.
10) Dyspnea (analyze it & see if it's related to SLE or not)  due to:
- Pneumonitis.
- Effusion, edema.
- Pulmonary infarction.
- Lung fibrosis.
- Myositis of respiratory muscles.
- Anemia  autoimmune (hemolytic).
In Lupus Pneumonitis:
- S.O.B.
- Fever  might present or not (suppressed by medications).
In Lung Fibrosis:
Patients may take bronchodilators  may benefit or may not.
5- Heart:
-Aseptic endocarditis (libman sack $).
-Pericarditis and pericardial effusion.
-Mitral regurge is more with SLE and Aortic regurge with RA.
6- Abdomen:
- Autoimmune hepatitis  high liver enzymes either due to drug or hepatitis.
- Pancreatitis  due to drug.
- Peptic ulcer  due to drug or vasculitis.
- Splenomegaly.
- Remember  felty's syndrome: Splenomegaly + RA + leucopenia + leg
ulcer.
- Diarrhea... because it can be associated with scleroderma  so they’ll have
esophageal dismotility and atonic intestine and blind loop syndrome…also
crest syndrome.
- 3 signs of peritonitis: fever – turbid drain – vomiting – abdominal pain (may
be).
7- Kidney: 50%
Lupus Nephritis  classes.
It could be:
a- Normal
b- Glomerulonephritis  5 stages (patterns):
• Minimal change GN.
• Mesangeal lupus GN.
• Focal proliferative GN.
• Diffuse proliferative GN.
• Membranous GN.
c- Renal failure.
d- Amyloidosis, but more with RA.
e- UTI.
8- Joints: >90%
-None deforming.
-Affect small joint.
-Distal interphalangeal joint.
-No morning stiffness.
9- Skin: 80%
- Butterfly rash.
- Discoid lupus erythematous (DLE).
- Livedo reticularis especially associated with antiphospholipid syndrome and
Pancreatitis
- Alopecia,
10- Hematologically:
- Any cytopenia.
- High ESR / CRP is normal in SLE.
- Low complements.
Investigations:
1- CBC  cytopenia …
2- High ESR which is indictor for reactivity.
Normal CRP in SLE  used in Differential Diagnosis
3- ANA which is sensitive / Anti-Ds DNA Antibodies which is diagnostic for SLE
AND Anti-sm Antibodies
4- LFT for chronic active hepatitis.
5- U & E for lupus nephritis.
6- Complements level  low.
7- Urine test  red cell cast And proteinuria  do 24h.
8- CXR  Cardiomegaly.
9- Echo.
10- ECG because of conduction abnormality and arrhythmia.
Signs of active disease:
1- Clinically: arthritis…fever, rash, pericardial and lung effusion.
2- Biochemical: cytopenia, low complements, high ESR and normal CRP. Also
active sediments in urine  hematuria or red cast cells.
Chest pain in a SLE patient is due to serositis  pleural effusion, pericarditis
Loin pain can be presented in SLE due to:
-Infraction (vasculitis).
-Infection.
-Renal vein thrombosis which is noticed as antiphospholipid syndrome (APS)
Normal ESR level up to 20mml/h
Zero ESR is seen in polycythemia.
In History:
 Dr Fat'h Al-deen likes this scenario when a student presents the History:
Is a patient is known to have SLE for 10 years Based on (mention the criteria that
was presented by the patient), thus upon them the diagnosis made and was
diagnosed by dr. ____ then she was admitted to the hospital with flare up of her
SLE complaining of ____
 Dr Fatmah Al-Beladi says "never say SLE alone"
Known as SLE,
- When was it diagnosed?
- What criteria are they based on?  Clinical & Laboratory.
- Treated with what?
- Complicated with what?
Always ask about chemotherapy, if the patient doesn't know  ask about: an
expensive tablets or drugs taken through IV once every month, because if she has
Lupus nephritis  class VI is usually treated by chemo.
Causes of death in a SLE patient?
1- Infections (opportunistic).
2- Renal /CNS involvement (active SLE).
3- Accelerated atherosclerosis  MI.
Differential diagnosis of SLE:
-RA.
-Scleroderma.
-Drug induced lupus.
-Rheumatic heart disease.
-Chronic active hepatitis.
Smart Rheumatology Qs by Dr. Fat'h Aldeen and then he swore when any
student answered them... He gave them almost a full mark 
SLE patient takes an anti-Malarial drug  like HydroxyChloroQuine?
The function of this medication is to suppress the high level of ANA and RF.
Side effect: Increased skin pigmentation and deposit in retina  and all these seen
only in high dose.
A patient came to Dr. Fat'h Al-deen, with symptoms similar to RA (joint pain), she
was diagnosed in Harvard as RA because she has High ANA and High sky RF.
So the doctor said “I don't trust Harvard University... I only trust in my knowledge
and trust excellent doctors" & told his patient that she doesn't have RA & gave her
anti-Malaria drug (hyrdoxyChloroQunine) because it suppresses for High ANA and
RF which then the symptoms subsides.
Then she was diagnosed to have parvovirus infection which causes symptoms
similar to RA & SLE.
How to differentiate that psychosis in SLE pt, whether it's
a side effect of cortisone or due to SLE it self?
 By test of Anti-Ribosomal B Abs  If positive so it is due to SLE.
So in both situations we've to decrease steroid because of psychosis that's
worsening.
Anti-phospholipids' Syndrome:
Diagnosed by Having Low platelets and prolonged PTT and in the Hx they've
abortions and Migraine, TIA, stroke, amurosis fugax. And in examination they've
levido reticularis.
Causes of prolonged PTT:
Either  coagulopathy or auto Abs like antiphospholipid $.
So to investigate anti-phospholipids' $  by three tests [ELISA]:
1- Lupus anticoagulant (its mechanism is very important)  see below:
2- Anti-Cardiolipin.
3- Anti-Beta 2 glycoprotein 1 Abs (beta2GP1)  very important for the
diagnosis.
50/50 fixed test for Lupus Anticoagulant:
Antiphospholipid pt. has prolonged PTT.
So, we take patient serum (50%) & mix it with serum from a normal person (50%).
If the result was corrected (PTT not prolonged), then the cause of prolongation is a
deficit in the blood itself (factor deficiency), not APLS. Because the defected blood
earned factors from the healthy blood.
If Prolongation of PTT is still the same  not corrected  Ag/Abs reaction
(autoimmune).
*In summary:
PTT:
-If corrected  factor deficiency.
-If not corrected  Ag/Abs.
Drug induced SLE:
-Usually by hydralazine – procainamide - IsoNiazid.
-They've Positive anti-Histone.
-Normal complements and ANA positive.
-Anti-ds DNA negative.
Methotrexate is hepatotoxic  it's given once weekly.
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