Rheumatoid Arthritis

Diagnostic Criteria for Rheumatoid Arthritis




Morning Stifness: morning stifness lasting at least 1h since the start of the stifness till the complete remision.

Arthritis in three or more joints: Arthritis in three or more joints regions of the fourteen following: metacarpophalageal, proximal interphalageal, wrists, eldbow, knees, anckles and metatarsophalangeal.

Arthritis in the hand: arthritis in the wrist, metacarpophalangeal and proximal interpahlangeal joints.

Symetric Arthritis: The arthritis is symetric and do not affect the lumbar region except the cervical region.

To this part of the list the symptoms has long at least six months.

Rheumatoid Nodules: Subcutaneous nodules in the joints or over bony prominences.

Rheumatic Factor: Rheumatic factor positive and Anti-CCP

Radiographs: Imaging tests indicating rheumatoid arthritis.

If > or = 4 there is Rheumatoid Arthritis diagnose and if the result is 2 the physician cannotexclude the diagnose.

Clinical aspects

There is historical description for rheumatoid arthritis and several presentation forms.

Z deformity: deviation at the wrist with ulnar deviation of the digits, often with palmar subluxation of the proximal phalanges.



Swan-Neck deformity: Flexion of distal interphalangeal joints and extension of metacarpophalangeal joints.

Boutoniere deformity: Extension of the distal interphalangeal joint and flexion of the proximal metacarpophalangeal joint.

Mallet finger: is a swan-neck deformity of the finger with loss of movility and pinch.



Hallux Valgus: is a foot deformity in which the toe has a lateral deviation.




Baker cyst: Is due to accumulation of sinovial fluid of the knee joint in the popliteal region.

SLE - Systemic Lupus Erythematosous

Diagnostic Criteria SLE

Malar Rash: Is a fixed erythema, flat or raised, over the nose, cheeks or forehead.



Discoid rash: Are an erythematous central patches normally raised with keratotic and scaly rims, atrophy scarring may occur.

Renal disorder: Proteinuria > 0.5 g/d, >3+ or cells casts.

Arthralgia: Joint pain in two or more peripheral joints, with tenderness, swelling or effusion.

Photophobia: Rash due UV rays.

Oral ulcers: Oral ulcers usually in the nasopharigeal region or in the oral mucose. Apthous like lessions.

Neurologic Disorder: Seizures or psychosis. Mood change.

Serositis: Pericarditis or pleuritis with effusion.

Cytopenias: Anemia, leukopenia, lymphopenia or thrombocytopenia.

ANA's: Antinuclear antibodies in serum tests or in immunofluorescence test.

Antibodies: Anti-dsDNA, Anti-SM and/or Anti-phospholipids.

If > or = 4 there is high probability to be a SLE patient with 95% sensibility and 75% specifity.

Note: the signs and symptoms could appear at any time of a well documented patient's history.

References

Harrison - Internal Medicine 17º Edition

STREPTOCOCCUS PNEUMONIE

STREPTOCOCCUS PNEUMONIE

Morphology

Is gram + coccus, facultative anaerobic, encapsulated, catalase -, alpha hemoliticus, has no movility, is no spore former, grows in chocolate agar and has 90 serotypes.

Colonies

This bacteria formes a mucose colonia, umbilicated ( with a central depretion) and do viridans hemolysis.

Virulence Factors

Adherence: the adherence to epitellium is mediated by surface proteins.
Capsule: Allow him to elude the immune response. is the most important virulence factor.
Peptidoglicane: Lipoteicoic and teicoic acid allows to ellicit immune response and make bigger inflamation due TLR5.
Coline Phosphate: links to PAF-R and allows the cell enter into the epitellium and elude opsonization and phagocitosis.
Pneumolisine: Is a citotoxic toxine, links to cholesterol and formes pores in the membrane of PMN, monocytes and lymphocites.
Autolisine: Is a protein that clives the peptidoglicane and bring outside the Hypometylated-DNA to performe a immune response due TLR9.

Clinical Manifestations

Neumonie: It's the princiapl manifestation in children and less prevalent in adults. The symptoms include fevere, dispnea, pleuritic pain, chills, night sweat, mucopurulent spute.

Another manifestations: Meningitis, Middle otitis, osteomielitis, sinusitis.

Dx

The diagnostic is performed with clinical manifestations, X-ray and laboratory tests.

Laboratory Tests

Gram Dyeing: With the well taken sputum of the patient, the sample is carried to the laboratory, and the best sample will be the one with: many bacterias, few epitellium and very immune complexes. The culture is only performed in the gram dyeing with mored than 25 bacterias and less than 10 epitellium cells.

Culture: Is performed in chocolate, blood and Mckonkey agar; in sterile recipient.

Antibiograme: Is very useful because of penicilline resistance. Also is very useful to confirme the bacteria with the optoquidine test.

Treatment: 3d generation Cephalosporine (e.g. Ceftriaxone). In resistent infections is useful a macrolide (e.g. Azytromicine) or a quinolone (e.g. levofloxacine)

ABDOMINAL INSPECTION

ABDOMINAL INSPECTION

The following images are an exposition part that i'd do.

When the doctor is doing the abdominal inspection, there are certain cases in which is possible speculate the diagnosis.

Courvoisier-Terrier Sign

If a patient had a visible and palpable gallblader and jaundice, the physician can think in pancreas head carcinoma with a 95% specifity. This is due to biliary duct obstruction by a mass.


Cullen Sign

If a patient has a periumbilical ecchymosis, got Cullen sign due to retroperitoneal bleeding that goes thorugh the falciform ligament, and pass till subcutaneus tissue due to conective tissue of the redondus ligament. This is unusual but indicate an acute pancreatitis.

Turner Sign

If a patient has a flank ecchymosis got the turner sign (also called Grey-turner). This happens due to para-renal space bleeding that goes with the quadratus lumborum muscle and pass through the flank muscle fascia, probably for a defect of the fascia. Lastly, the blood pass through the subcutaneous tissue. This is also unusual and indicate acute pancreatitis.


Erythema Ab igne

If a patient has a brown livedo reticularis-like pigmentation, the doctor could think in two possible options: a physical damage of the skin (e.g. heat exposure) and a chronic pancreatitis.




Sister Mary Joseph's Nodule

Metastasic cancer of the umbilillicus associated with gastrointestinal and ovarian tumors. This condition was named for Sister Mary Joseph (1856–1939), a surgical assistant for Dr. William
Mayo, who noted the association between paraumbilical nodules observed during skin
preparation for surgery and metastatic intraabdominal cancer confirmed at surgery.



References

- Sopeña Bernardo et all; Visible gallbladder. Medical images; 2007

- Mok Daniel H M et all; Erythema Ab igne in chronic pancreatitis: a diagnostic sign; Journal of royal society of medicine; 1984

- Mookadam Farouk et all; Cullen’s and turner’s signs; NEJM; 2005

- Kanter, Judith et all. Sister Mary Joseph's Nodule - NEJM

Mycobacterium tuberculosis

MYCOBACTERIUM TUBERCULOSIS

IS a weak gram + bacteria, aerobic, facultative intracelular, no movility, no capsule and no spore former. Is alchol acid resistant bacilli and has a very width cellular wall. The wall consist in N-acetyl glucosamine, arabinose polymers, mycolic acids, glicolipids and lipoarabinomanam.




Virulence

Cordon factor which is a mycolic acid is very immunogenic and interrupts fagolisosome fusion and electron transporter chain. Lipoarabinomanam is an immune-modulator that elicits inflammatory response due TOLL like receptors. Bacterian urease adjust cytoplasmic ambient becoming alkaline allowing his survival.

The infection occurs when a patient elicits bacilli in aerosol shaped secretions, the bacilli arrives to the alveoli and is phagocitated by dust macrophages, this cell is not able to destroy it so travel to the hiliar nodes in the lymphatic system creating ghon complex, which is a calcificated and fibrous node. This action constitute the first stage, the second is spread via bloodstream to other organs. The thirs stage is very slow, and is very usual with pleurisy. The latest stage constitutes the resolution in which the patient stops the bacilli colonization.

The macrophage with the bacilli is surrounded by other inflammatory cells and dies becoming caseose forming granulome, with lymphocytes CD4 and Cd8, fibroblasts and giant cells. This stoping situation is the normal, but when is immune depletion the bacilli can become wild again and multiply. HIV can elicit bacilli reinfection, so is very normal this co-infection.

Clinical manifestations

There is a wide spectrum of disease’s ways.

1º pulmonary TB: is more frecuent in children and affects the middle and lower lobes of the lungs, is usually accompanied by pleural effusion . It occurs when the infection with bacilli is new. There are lymphatic nodes in the hilious region.

Pulmonary Tb pos-first: Is usual in adults and affects more frequent the apex because of the major oxygen ability, it can cause cavitations with abces and necrosys regions. There are lymphatic nodes that can compress the bronchium and elicit collapse of a lung segment. Is very usual due to reactivation of the bacilli. Clasical symptoms include: fever, malaise, night sweat, weight loss, comsumption and anorexy. Hemoptisys and anforic bruit are very frequent. Tha X-ray shows bilateral infiltrate and nodes in the hilio.

This Image shows a bilateral and nodular infiltrates on the superior left lung. There is an air-level in the low right lung. (Cortesy of NEJM)

Extrapulmonar TB: Can affect the nervous system, digestive system, cutaneous lesions, millliar disease, bone and articulation lesions (pott’s disease) and only lymphatic nodes affection (Scrafula).

Vaccination

Is a replicative vaccine and consists of BCG attenuated that bring immune contact and allow the immune system his recognition and resolution of the infection.

Dx

The diagnosis is with the culture of sputum and PPD test, X-ray, clinical manifestations.

Treatment

Isoniazide
Rifampicine
Piperazinamide
Etambuthol

HIV

HIV

HIV is virus that belongs to retroviruses and more specifically to lentiviruses, is enveloped and contains two RNA strains with positive polarity. His genome is composed by 9 genes clasificated in 3 groups: structural genes: gag, pol, env; regulatory genes: tat, rev; accessory genes: vpr, vpu, vif and nef. Gag genes code for core proteins which consists of p24, p17 and p7. Env codes for envelope proteins which consists of gp120 (surface protein) and gp41 (transmembrane protein). Pol codes for protease, integrase and reverse transciptase.

Tat gene codes for a genome binding protein that ensures the full-transcription of the viral genome, and rev is a protein that allos virus pass through early to late phase, this protein links immature ARN without splicing and take it outside nucleus.

Nef genes encode a protein that inhibits CD4+ and MHC-1, vpr is a transporter protein that inserts itself in every cell membrane, allowing virus infect non-dividing cells, translocate the preintegration complex through the nucleus and eliciting apoptosis by his insertion in the mitochondrial membrane. Vif are essencial for viral transcription and VPU destroy the CD4+ like Nef.

Infection

The infection occurs in every cell with CD4+ and co receptor: CCR5 or CXCR4 in macrophages or lymphocytes respectively. But the first contact is with the DC via DC-sign this cell carry the virus to a lymphatic node where meets the susceptible cells. The gp 120 links the CD4+ and the co receptor and change the conformation allowing the gp41 bring the hydrophobic domain for membrane fusion. When the virus enter the cells is decapsidated and laves the RNA and constitutional proteins in the cytoplasm, the reverse transcriptase converse the RNA to DNA, then the integrase cuts the genome limits allowing the insertion in the host genome, where the protease cut the new RNAm in small peptides that constitutes the viral proteins. The viral genome replicates and destroys the host cell bringing new virions.

There are two types of HIV phenotypes: R5 and X4, R5 occurs when the virus infects first macrophages and X4 when infects lymphocytes. X4 is more aggressive and develop very quickly toward AIDS.

The pathogenesis is explained by cell lysis and the mechanisms are three: apoptosis, depletion by immune system and delayed lymphocytes regeneration.

Buerger's Disease - Obliterant Thromboangitis

Obliterant Thromboangitis (Buerger’s Disease)

Obliterant tromboangitis is an occlusive vascular disease that comprises middle and small arteries, and distal extremities veins. His prevalence is bigger in Asian population and masculine population with less than 40 years. There is no evidence about the cause but there is an association with cigarettes.

In the lesion place are polymorphic nuclear cells. Later, arrives monocytes, fibroblasts and giant cells. In advance disease is very frequent perivascular fibrosis. There is no intime layer compromise but it can be thrombus formation.


Clinical

The patient with tromboangitis presents a triad: extremity claudication, Reynaud phenomena and migrans thrombo-phlebitis. The patient conserves the humeral and popliteal pulse, but radial, ulnae and pedis pulse are absent. It can present nail atrophy, vessels ulcers and gangrene lesions. Therefore, extremities claudication is localized in calf and feet, and superior extremity claudicate on the hand and forearm.

The first image shows a patient with a hanged-foot and the second after elevation.




Dx

The diagnostic is via excicional biopsy and pathological study. Arteriography is very useful.

Treatment

There is no treatment; the only recommendation is to cease smoking, while this neither warranty nothing cause probably won’t improve. Can proceeds with angioplasty derived from big arteries. Anticoagulation and corticoids doesn’t work.

References: Harrison - Intern Medicine - 16º Edition.