Short Q
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1.To understand the etiology and the
pathogenesis of HDN ?
Etiology - Caused by blood type incompatibility between mother and
fetus.
Pathogenesis :-
1. Hemolysis of ABO blood type incompatibility can occurred at first
fetus.
2. Hemolysis of Rh blood type incompatibility occurred at second orlater fetus.
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3. Diagnosis and the treatment of HDN ?
Diagnosis :-
1Hemolysis of ABO blood type
incompatibility:
The antibody release test result is positive
usually.
2
Hemolysis of Rh blood typeincompatibility
The direct Coombs test is positive usually.
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Treatments:
Premature treatments :-
Premature delivery:
If labor is induced, fetal lung maturity must be determined
using the lecithin/sphingomyelon (L/S) ratio (thin layer
chromatography) to avoid respiratory distress syndrome Plasmapheresis :
For the pregnant mother unsuitable the premature delivery.
Intrauterine blood transfusion:
If fetal hydrops or fetal Hb
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Neonatal treatments: -
Phototherapy
Exchange Transfusions
Pharmacological agents
Other treatments : -
Prevention of hypoglycemia,hypothermia.
To correct hypoxia,anemia,edema and heart failure.
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4. Definition :-
Billirubin encephalopathy
Neurologic syndrome resulting from the deposition of
unconjugated bilirubin in nucleus basalis.
Main cause due to hemolytic disease.
Caused by any other disease with unconjugated
hyperbilirubinemia.
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5. Clinical manifestations and diagnosis of
Bilirubin Encephalopathy ?
Warning stage: lasts about 12-24hrs.
Spasm stage: lasts about 12-48hrs.
Convalescent stage: lasts about 2weeks.
Sequelae stage
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Warning stage of BE
Lethargy
Low response
Sucking weakness
Weak sucking and moro reflexing
Vomiting
Reduced muscle tone
Severe jaundice
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Spasm stage
Convulsion
Opisthotonos and fever
Increased muscle tone
Apnea
Stiffly extending his of her arms inward rotation with fists
clenched or even opisthotonos
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Convalescent stage
Nursing and reaction improvement
Reduction of seizure frequency
Opisthotonos gradually disappeared
Muscle tone gradually recovered
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Sequelae stage:BE of tetralogy
Athetosis
Limitation of eyes movement
Hearing impairment
Enamel dysplasia
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6. Therapy of BE ?
Phototherapy
Plasma or albumin
Exchange transfusion
Enzyme inducer: phenobarbital
Original diseases treatment
The other symptomatic treatment
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7. How do we avoid the bilirubin
encephalopathy for HDN infants?
Declining jaundice quickly is necessary 4 HDN
infants 2 avoid BE .
Phototherapy
Exchange transfusions
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8. whats the characteristics of physiologic
jaundice
The characteristics of physiologic jaundice : -1Jaundice appears at 2~3 days.
2Full-term neonates jaundice declines to adult levels
within 14d. Prematures jaundice usually delays to 3~4 wkof age.
3Bilirubin level of blood serum < 222~257 mol/L
4Conjugated bilirubin level of blood < 34 mol/L
5Bilirubin level of blood serum increases every day
< 85mol/L.
6General condition of the baby is well.
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9. Whats the characteristics of pathologic
jaundice?
The characteristics of pathologic jaundice :-
1Appear too early
2Degree too severe3Duration too long
4Progress too rapid
5Again appeared after it subsided
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10. Treatment of neonatal jaundice ?
Phototherapy
Light source : spectral outputs 420 500 nm
Exchange transfusions : -
Remove antibody
Remove bilirubin
Correct anemia
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11. Differences between physiologic jaundice
and pathologic jaundice ?
Refer to slide 16- 17.
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12. Indications & Complications of
Phototherapy ?
Phototherapy : Lipid unconjugated bilirubin water- soluble isomeride- Light source: Spectral outputs 420 to 500nm
Side effects of phototherapy :
a. Diarrheab. Fever
c. Skin rash
d. Bronze baby syndrome
(Conjugated bilirubin > 4mg/dl)
e. Riboflavin reduction
f. Dehydration and Hypocalcemia
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13. Diagnosis test of HDN ?
Sensitized erythrocytes and blood group
antibodies determination:
Coombs test : Red blood cells sensitized.
Antibody releasing test : Sensitivity test to detect
sensitized erythrocytes.
Blood type antibody test in the infant serum.
Blood type antibody test in the maternal serum.
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14. Pathophysiology of Rh ?
Pathophysiology :-
Seizures etc.
Red blood cell breakdown
Hyperbilirubinemia
Jaundice
Kernicterus
Anemia
1. Liver
2. Spleen
3. Heart, other organs
4. Hydrops
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15. Indications of Exchange Transfusions ?
Indication of transfusions:
one of the follows
a. 20mg/dl (340 mol/L)b. > 4mg/dl,Hgb
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16. Causes of neonatal hypoxic ischemic
encephalopathy ?Causes
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17. Pathology & Pathophysiological changes
of neonatal HIE ?
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Pathophysiology
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18. Clinical features of neonatal HIE ?
Muscle tone and deep tendon reflexes
Behavioral abnormalities
Neonatal reflexes Apnea and seizures
Stupor and ventilatory support
Ocular motion and pupils
Heart rate and blood pressure
Outcome
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19. Differential diagnosis of neonatal HIE ?
Methylmalonic Acidemia
Propionic Acidemia
Urea cycle defects Zellweger syndrome
Mitochondrial disorders
Neuromuscular disorders Brain tumors
Developmental defects
Infections
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20. Treatment of neonatal HIE ?
Medical Care : -
Initial resuscitation and stabilization
Supportive care: mechanical ventilation
Perfusion and blood pressure management
Fluid and electrolytes management
Hyperthermia management
Treatment of seizures
Surgical Care
Consultations
Diet
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21. Prognosis of neonatal HIE ?
Lack of spontaneous respiratory effort
The presence of seizures
Abnormal neurological findings
Abnormal EEG background
Feeding difficulties
Poor head growth
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22. Diagnosis criteria of bacterial
meningitis ?
Confirmation of the diagnosis: isolation from the CSF of a specific
bacteria pathogen by microscopy or a positive culture or rapid
antigen-detection test of CSF
Gram-stained smear of CSF: identify the causative organism in
70-90% of cases
CSF culture: positive in about 80% of cases. Definitive
diagnosis, determination of antibiotic sensitivity.
PCR: amplifies bacteria DNA(H influenzae, N meningitidis)
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23.Symptom of purulent meningitis ?
Fever
Headache
Vomiting
Increased ICP
Meningeal Irritation
Anorexia
Malaise
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25. Treatment of Meningitis
Antibiotic : Penicilln,Ampicillin,ceftriaxoneCorticosteroid : Dexamethasone
Mannitol
General and supportive measure
Maintenance fluid and thermal energy supplement.
Fluid administration: 60-80ml/kg.d
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26.Complication of epilepsy ?
1.Mental retardation
2.Loss of hearing
3.Impairment of visual area
4.Motor and sensory deficits
27 T b l M i i i
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27. Tuberculous Meningitis
(Manifestation)
Increased Intracranial Pressure
Cranial Nerve Injury
Meninges Irritation Signs
Cerebral-Parenchyma Damage
Spinal Cord Damage
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Pneumonia (Manifestation)
Tachypnea, Dyspnea,
Retractions,
Grunting,
Nasal flaring,
Cyanosis and the presence of rales or rhonchi on physical examination.
Lethargy,
Poor feeding,
Fever, temperature instability,
Apnea,
Tachycardia,
Poor perfusion,
Metabolic acidosis
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Tuberculosis Symptoms
Perpetual Cough
Fever
Weight loss
Night sweats
Loss of appetite
Fatigue
Pain while breathing
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Diagnosis of TB
Tuberculin skin test
Chest X-ray
Physical examination
Serological (blood) test
AFD test (collect sputum to smear and culture
it)
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TREATMENT FOR ACTIVE TB
A combination of the following four antibiotics are the mostcommonly used, however are not risk free:
rifampicin R
It may cause fever, rashes, liver damage, and in some rare cases has
led to death.
isoniazid H It may cause rash and abnormal liver function tests.
ethambutol E
It may cause Red-green color blindness and loss of vision
pyrazinamide Z
It may cause joint pains, nausea, vomiting, skin rash,, malaise, and
fever
When taking antibiotics, overdose and underdose is a problem
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Treatment for TB meningitis
Antituberculosis drugs
Corticosteroids
Decrease intracranial pressure
Ventriculoperitoneal shunting
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Questions
What is diagnostic criteria of nephrotic syndrome?
How to distinguish the differences between simple type and
nephritic type?
What are causes of the nephrotic syndrome ?
What is histology of primary nephrotic syndrome?
What are major complications of nephrotic syndrome?
How to treat nephrotic syndrome?
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Diagnostic Criteria
1. Nephrotic range proteinuria proteinuria(>50mg/kg/day)
Urine protein 3+ or 4+ by dipstick testing
2. Hypoalbuminaemia
serum albumin less than 25g/l
3. Oedema
The onset is insidious , with swelling around the eye and facial
puffiness .Over the next few days ,it gradually increases to involve
the extremities and abdomen
4. Hyperlipidemia
Serum cholesterol more than 5.7mmol/l
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Difference
1. Nephrotic syndrome is a disease of the kidney whilenephritic syndrome is a disease of the glomeruli. Nephriticsyndrome is also called glomerulonephritis.
2. Nephrotic syndrome manifests the classic symptoms, suchas: edema, proteinuria, hypoalbuminemia, andhyperlipidemia. Nephritic syndrome manifests the sameexcept there is an accompanying blood in the urine.
3. Diagnosis for nephrotic syndrome is a 24-hoururine/protein measurement and lipid profile while anephritic syndrome involves an ASOT, urine tests, andblood tests.
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Main causes of nephrotic syndrome (NS) in children
Primary nephrotic syndrome
Secondary nephrotic syndrome (Multisystem diseases )
Henoch-schonlein purpura Systemic lupus erythematosus Hepatitis B
Congenital nephrotic syndrome
Idiopathic CNS of Finnish type Diffuse mesangial sclerosis
Secondary Congenital syphilis
Toxoplasmosis Cytomegalovirus
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Histopathologic classification
Minimal change diseases (MCD)
Pure minimal change diseases
MCD with mesangial proliferation (MesPGN)
Focal segmental glomerulosclerosis(FSGS)
Membranoproliferative glomerulonephritis(MPGN)
Membraneous nephropathy(MN)
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Major Complications of Nephrotic Syndrome
Infection
Hypovolaemia
Thrombosis
Hyperlipidaemia
Acute renal failure
Side-effects of drugs
Corticosteroids
Alkylating agents
Cyclosporin A
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Management
Cyclophosphamide (CTX) CTX2-3mg/kg/day po for 8-12weeks ,or iv pulse CTX 0.5/m2
Cyclosporine (CsA)
Dosage of 5-6mg/kg/day to maintain the whole blood trough level
at 80 to 120ng/ml
Tacrolimus (FK506)
0.1mg/kg/day in BD doses
Trough level maintain at 5-10mcg/l
Mycophnolate mofetil (MMF)
Dosage 250-1200mg/m2/day in 2 doses
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Supportive Therapy
To minimize infection(vaccination and prophylactic antibioticcs )
To minimize risk of thrombosis
( hydration; and avoiding prolonged immobilisation)
To maintain nutrition ( high biological value protein intake ) To treat edema and hypertension
To treat hypercholesterolaemia (low cholesterol diet and lipidlowering agents)
To reduce proteinuria (ACEI or angiotensin 2 receptor blockers)
To avoid the use of nephrotoxic drugs
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General Symptoms Acute
Glomerulonephritis
Fatigue
Abdominal pain: more than half
Low-grade fever
Loss of appetite Nausea
Vomiting
Headache
Hematuria
Proteinuria
Edema Hypertension
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Lab Investigation A.G.
Urinalysis
Blood test
Blood Chemistry
Serological testing
Complement level (C3,C4)
Renal Ultrasound
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Treatment AG
Restriction
Salt
Fluid intake
Control of hypertension
Diuretics (Furosemide)
Anti hypertensives
Dialysis
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1.Inadequate storage: Premature
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Anemia three types:
Anemia of inadequate production
Hemolytic anemia
Blood loss
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1.blood filmhypochromic and microcytic2.bone marrow samplingThe bone marrow is hypercellular, with erythroid
hyperplasia,The normoblasts.may have scanty, fragmented cytoplasm with
poor hemoglobinization.
3.iron metabolism:
Iron study ID IDE IDA*serum ferritin(SF) (