Wednesday, October 30, 2013

SYSTEMIC LUPUS ERYTHEMATOUS part 2

SYSTEMIC LUPUS ERYTHEMATOUS part 2


  • autoimmune ? antibody fails to recognize the body's own cells
  • As a result ? caused inflammation in the body
  • In systemic lupus arise keradangannya
  • Antibodies are found : ANA , ds DNA , anti- Ro , anti- La , and anti- RNP .
Systemic Lupus Erythematosus

Mechanisms of autoantibody production in SLE ​​and APS 

Mechanisms of renal damage by anti - DNA antibodies

Classic picture :
-          young woman ,
-          fever ,
-          buterfly rash,
-          lymphadenopaty ,
-          joint pain ,
-          alopecia ,
-          pleural effusion ,
-          edema + Uriah protein

Not all patients gave a clear clinical picture , sometimes only one or two symptoms for months , and then the other symptoms are more obvious

Non-specific symptoms
At first the symptoms that usually preceded by non-specific
  • fever
  • nausea
  • Vomiting
  • appetite down
  • Weight loss
  • Fast tired
Results: Sle patients who are hospitalized in Soetomo april - september 2003 ( 98 patients )
Weight down
67.3
Tired
84.7
fever
53


SYSTEMIC LUPUS ERYTHEMATOUS Part 1


SYSTEMIC LUPUS ERYTHEMATOUS
Definition
Lupus :
- autoimmune diseases
- Acute and chronic
- multisystem
- there is some form of clinical :
  1. systemic (SLE), 
  2. discoid (DLE, scarring rash only),
  3. drug-induced (DILE),
  4. neonatal (NLE).
General :
  • autoimmune multisystem disease
  • prevalence 1 in 2,000
  • 9 to 1; female to male (1 in 700)
  • peak age 15-25
  • immune complex deposition
  • photosensitive skin eruptions, serositis, pneumonitis, myocarditis, nephritis, CNS involvemen
The incidence
  • > ratio of 9:1, age 15-45 years
  • black> white
  • Surve IN USA à 1,500,000 people
  • Chronic inflammatory factors trigger yet dikeyahui responsesà
  • SLE: results of a complex interaction between genetic and environmental factors
  • Environmental factors: infections, antibiotics, ultraviolet light, extreme stress, certain drugs, hormones
  • certain drugs suspected drug activity meningkarkan immune response or reduce the immune response procainamide, hydrazaline,

Saturday, October 26, 2013

CHOLERA


CHOLERA
Cholera is an acute infection of Vibrio cholerae uses subtle clinical profus characterized by diarrhea and vomiting , which quickly lead to progressive dehydration and shock , due to infection . Vibrio eltor can also cause the same disease .

CONTAGION
Infectious materials
- Water , contaminated food
- V. eltor may live long in the water and food

Transmission source :
- Patients mild infection , asymptomatic carrier
- Cholera asiatica : Asymptomatic : Clinical = 4 : 1
Cholera eltor : Asymptomatic : Clinical = 10 : 1
( iceberg pnenomenon )
- All ages are susceptible to cholera
- Endemic areas : child > adult , male > female
- Immunity : type humoral

PATHOGENESIS AND PATHOLOGY
oral transmission
Through the gastrointestinal acid ( alkaline ) producing enterotoxin
attached to the intestinal mucosa 10-30 minutes later secretion of fluid
adenyl cyclase maximum : 3-4 hours lasts 8-12 hours
No mucosal damage

Enterotoxin adenyl cyclase stimulating intestinal secretion of isotonic fluid along the bowel ( cyclic AMP increases )

No effect on gastric secretion ; absorption colon
Isotonic faecal material ; K 4 times ; bikarbonas 2 times
Secretion Speed ​​: 1,000 cc / hour ; longer without antibiotics : 5 days

CLINICAL MANIFESTATIONS
Severe disease varies : mostly asymptomatic , mild diarrhea

INCUBATION TIME : 2-6 DAYS :
• Starting watery diarrhea , abundant , without mules , without
   tenesmus
• Feces turns white liquid , turbid , odorless foul / fishy , smells
  sweet, like rice water
• Vomiting after diarrhea ; muscle spasms ( due to electrolyte
  disturbance )
• Symptoms of loss of water , electrolytes , acidosis
• Signs of dehydration : hoarse voice ( vox Cholerica ) , sunken
  eyes, dry lips , sunken abdomen ( scaphoid ) , wrinkled fingers
  ( hand washer )
• Signs circulatory disorders ; metabolic acidosis

DIAGNOSIS
CLINICAL :
Dx cholera in endemic areas is easy , light , whereas outside the endemic area Dx > hard stools often , without nausea / mules , normal temperature , such stools washing rice , fast backward state due to dehydration , shock and acidosis

BACTERIOLOGICAL :
Rectal swabs , preserved in transport media

DIAGNOSIS :
- Vibrio cholerae
- Clostridium perfringens
- Staphylococcus aureus
- Escherichia coli
- Bacillus cereus

DEHYDRATION
Dehydration criteria : use of clinical methods
1 . Pierce method is based on clinical signs of dehydration :
    - Mild dehydration : 5 % BB liquid needs
    - Dehydrated medium : 8 % BB liquid needs
    - Severe dehydration : 10 % BB liquid needs
2.Pemeriksaan Plasma Specific Gravity : the solution zn Cupri
  sulfate or Refraksimeter

TREATMENT
CAUSAL AND SYMPTOMATIC SIMULTANEOUSLY
- Rehydration in 2 stages: initial rehydration; maintenance
- Infusion therapy on;
   * Severe dehydration, hypovolemic shock, uncontrollable vomiting,
      severe complications
- Cases of mild and moderate: Oral rehydration with oral material
- Criteria dehydration: using clinical methods, CVP, BJ Plasma
          BJ Plasma - 1,025
          Fluid deficit = x B x 4 ml
                          0001
Antibiotics: tetracycline 50 mg / kg divided into 4 doses of co-trimoxazole

PREVENTION
Hygiene and sanitation improvement
- Repair dining facilities - drinks
- Immunization:
- Standard Mixture: 10 billion vibrio die,
- Protection 60-80% in the past 3-6 months