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3. SAQ (1) Flashcards

1
Q

⭐Characteristics of Bilirubin metabolism in a Newborn

A
  • Increased Bilirubin Synthesis ↑
  • Less effective Binding and Transportation of Bilirubin
  • Premature Hepatic Function
  • Enhanced Absorption of Bilirubin via the Enterohepatic Circulation
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2
Q

⭐ Characteristics of Rotavirus

A
  • Acute Diarrhea occurred in infants b/w 6 months – 2 years age
  • Mostly in Autumn and Winter
    o 1-2 days – Fever, Upper Respi. Tract Infection and Vomiting
    o 3-8 days – Profuse Watery Diarrhea
  • Dehydration and Acidosis are common
  • Stools are
    o Profuse
    o Frequent
    o Watery
    o Yellow-water/egg-soup like w/ small amt. of Mucus
    o Mostly stool are Normal under Microscope w/o Blood (RBC) or Pus (WBC)
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3
Q

⭐How to Diagnose CHF in child with Severe Pneumonia

A
  • Tachypnea >60/min
  • Tachycardia >180/min
  • Extreme Agitation with Cyanosis and/or Duskiness
  • Soft Heart Sound, Gallop Rhythms, and Engorgement of Neck Veins
  • Rapid Hepatomegaly
  • Oliguria, Anuria, Edema of the face or extremities
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4
Q

⭐Typical Bone Deformity in Active Stage in Rickets of Vitamin D deficiency

A
  • <6 months
    o Lesion mainly at Skull
    o Craniotabes
    o Ping-pong ball sensation
  • > 6 months mainly Osteoid Tissue accumulation o Rachitic rosary
    o Widening of wrists (bracelet) and ankles (anklets) o Caput quadratum
    o Wide open Anterior Fontanels
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5
Q

Definition of Iron Deficiency Anemia (IDA)

A
  • IDA is a Microcytic and Hypochromic Anemia caused by Iron Deficiency
  • Age: 6-24 months
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6
Q

Classification stages of Iron Deficiency Anemia (IDA)

A
  1. Iron Depletion (ID)
    - Reduced Iron Store
    - Normal iron supply for Hematopoiesis
    - Normal blood Hb value
  2. Iron Deficient Erythropoiesis (IDE)
    - Reduced Iron Store
    - Reduced iron supply for Hematopoiesis
    - Normal blood Hb value
  3. Iron Deficiency Anemia (IDA)
    - Reduced Iron Store
    - Reduced iron supply for Hematopoiesis
    - Reduced blood Hb value
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7
Q

Differences from Physiologic Jaundice from Pathologic Jaundice

A

(photo)

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8
Q

Classification (Birth Weight, BW)

A
  • Macrosomia: >400g
  • Normal BW: 2500-4000g
  • Low BW (LBW): less than 2500g
  • Very Low BW (VLBW): <1500g
  • Extremely Low Birth Weight (ELBW): <1000g
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9
Q

Diagnosis of Iron Deficiency Anemia (IDA)

A
  • Clinical Manifestation
    o Age 6-24 months
    o Pallor, Fatigue, Dizziness o Tinnitus,
    o Spoon-shaped nails
  • Extramedullary Hematopoiesis
    o Hepatomegaly & Splenomegaly o Lymphadenosis
  • Blood Examination
    o Low Hemoglobin and Iron Level
    o Blood Smear microcytic and Hypochromic anemia
    o Bone marrow -> an increased number of Erythroblasts with delayed
    maturity of Cytoplasm
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10
Q

Treatment of Iron Deficiency Anemia (IDA)

A
  • General measures
    o Special nursing o Avoid infection
  • Etiologic treatment
    o Increased dietary intake of Iron
    o Treatment of Hookworm disease, Chronic diarrhea
  • Iron supplement
    o Oral dose of elemental iron is 4-6mg/kg/d in three divided daily doses
  • Efficacy observation
    o Blood Hb Level begins to increase in 2 weeks after Iron therapy o Symptom and signs completely resolve within 4-6 weeks
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11
Q

Definition of Congenital Heart Disease (CHD)

A

Congenital Heart disease is defined as an abnormality in circulatory structure or function that is present at birth
- Ventricular Septal Defect – VSD
- Atrial Septal Defect – ASD
- Patent Ductus Arteriosus – PDA
- Pulmonic Stenosis
- Coarctation of the Aorta
- Transposition of Great Arteries
- Tetralogy of Fallot

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12
Q

Classification and Main Diseases of Congenital Heart Disease (CHD)

A
  • Acyanotic
    o L-R shunt: VSD, ASD, PDA o R-L shunt: ToF, T4, TOA
    o No shunt: PS, AS, CoA
  • Cyanotic
    o Pulmonary blood flow decreased: TOF
    o Pulmonary blood flow increased: TGA, TAPVR
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13
Q

Complications of CHD

A
  • Developmental Problems
  • Respiratory Tract Infections
  • Endocarditis
  • Pulmonary HTN
  • Heart Rhythm Problems
  • Heart Failure
  • Blood Clots
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14
Q

Diagnosis and Treatment of CHD

A
  1. Diagnosis of CHD o History
    o Physical Examination
    o Collect information from ECG, CXR, Echocardiogram,
    Angiocardiography 2. Treatment of CHD
    o ASD
    § Surgical or Transcatheter Device cLOSURE
    § Time for Elective Closure
    * After the 1st year – before entry to school
    o VSD
    § Small VSD monitored until VSD closed
    § Large VSD control Heart Failure – prevent development of
    Pulmonary Vascular disease
    § Surgery
    o PDA
    § Irrespective age, pts. With PDA needs surgical/catheter
    closure
    o ToF
    § Depends on severity of Right Ventricular Outflow Tract
    Obstruction
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15
Q

Etiology of CHD

A
  • Genetic factor (internal factor) o Gene mutation
    o Chromosome aberration
  • Environmental factor (external factor)
    o Viral infection
    o Maternal diabetes
    o Alcohol consumption
    o Other maternal teratogen exposure
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16
Q

Moderate and long-term steroid therapy in Nephrotic Syndrome

A
  • Moderate to Long term
    o Everyday – 2mg/kg/d o Every other day – 4w
    o Tapped everyday – 2-4w is 0.5-1mg/kg x 3m Moderate is more than 6 months
    Long is more than 9 months
  • Short term – Prednisone
    o Everyday – 2mg/kg/day divided into 2-3 dose/4wks
    o Every other day – 1.5mg/kg/d every other morning/4wks
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17
Q

Causes of Rickets of Vitamin D

A
  • It’s a Calcium and Phosphorus disorder caused by insufficient vitamin D in the body of children
  • Leading to insufficiency of mineralization in Metaphysis of Long Bone and Bone Tissue
  • Bone change at the part of rapid growth bone
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18
Q

Characters of different stages of vitamin D deficiency rickets

A
  1. Initial stage (Early stage)
    - Non-specific psychiatric symptoms
    - Neuro-excitability is increased
    - Irritability, anxiety, alopecia
  2. Active stage (Excitation period)
    - Bone change
    - Usually in pts <6 months
    - Lesion @ skull
    - Craniotabes
    - Ping-pong ball sensation
    - If pts >6months, pts may have accumulation of osteoid tissue
  3. Recovery stage
    - Clinical symptoms gradually disappear after sun-shining or treatment
  4. Sequelastage
    - Common in children >2 yrs old
19
Q

3 Signs in patients with Latent Tetany of Vitamin D deficiency

A
  1. Chovstek Sign
    - Twitching of Homolateral facial muscles due to Hyperexcitability of the
    Facial Nerve Anterior to the ear as it crosses Zygomatic arch elicited by
    tapping lightly over it 2. Peroneal Sign
    - Elicited by tapping Peroneal n. below Head of Fibula while the knee is relaxed and slightly flexed. A (+) response will cause Dorsal Flex and Abdutction of foot
  2. Trousseau’s Sign
    - Carpopedal spasm induced by Ischemia 2ndary to inflation of
    sphygmomanometer cuff commonly to an individual’s arm to 20mmHg over systolic blood pressure for 3mins
20
Q

Treatment of Tetany (Vitamin D deficiency)

A
  • First aid treatment
    o Convulsion – O2 administration
    o Laryngospasm – pull the tongue out of the mouth, mouth to mouth
    respiratory resuscitation and sac pressure oxygen inhalation
    o Control convulsion and laryngospasm – 10% chloral hydrate; 0-4-0.5
    ml/kg e.a
    § Ca agent – 10% Ca gluconate 5-10ml + 10% Glucose liquid 5-
    20ml
    § Vitamin D – oral administration of Vit D, according to them
    methods
21
Q

Severe Manifestation of Acute Glomerulonephritis (AGN)

A

. Hypertensive Encephalopathy
- Approx 5% of hospitalized children
- HTN usually severe, accompanied by CNS dysfunction (e.g headache, vomit,
depressed sensorium, confusion, visual disturbances, aphasia, memory loss,
coma, convulsion)
2. Circulatory Congestion
- Dyspnea, orthopnea, cough – present
- Pulmonary Rales often audible
- Patient with otherwise normal Cardiovascular system, Cardiac failure is
unusual
- Pallor is common at onset and is not explained entirely by Anemia
3. Acute Insufficiency
- Glomerular inflammation (e.g Cellular Prolfieration, Edema)
- Capillary loop is narrowed
- Glomerular Filtration reduce

22
Q

ABCDE resuscitation for treatment of Asphyxia of Newborn

A
  1. A (Airway)
    - Establish open airway
    - Position of the infant (no extend/flex)
    - Suction mouth, nose
    - Suction any blood, secretion
    - Placing a guedel airway
  2. B (Breathing)
    - Initiate breathing
    - Tactile stimulation
    - PPV if necessary (+ press ventilation)
    - Mask ventilation placed over mouth and nose
  3. C (Circulation)
    - Maintain circulation
    - Stimulate cardiac compression
  4. D(Drugs)
    - Adrenaline -> low HR
    - Sodium bicarbonate acidosis
    - Naloxone bradypnea
  5. E (Evaluation)
    - Respiration – if none/gasp, give PPV 21% oxygen 15-30 sec
23
Q

Neonates Asphyxia

A
  • Asphyxia
    o Failure to initiate and maintain spontaneous respiration
  • Hypoxia + Hypercapnia + Metabolic Acidosis (combination)
  • Might lead to Irreversible Brain damage
24
Q

Neonatal Asphyxia Evaluation (APGAR Score)

A

(pic)

25
Q

Criteria for Perinatal Asphyxia

A
  • Prolonged Metabolic or Mixed Acidemia (pH <7) on an Umbilical Cord Arterial Blood Sample
  • Persistence of an APGAR Score of 0-3 for >5 mins
  • Clinical neurological manifestations (e.g Seizure, Hypotonia, Coma, or HIE in
    immediate neonatal period)
  • Evidence of multiorgan system dysfunction in immediate neonatal periods
26
Q

Management for Neonatal Asphyxia

A
  1. Preparation for Resuscitation
    - Anticipation of high risk delivery
    - Proper equipment
    - Trained personnel
  2. Purpose of Resuscitation – reverse Asphyxia before irreparable damage occurred
27
Q

3 Assesment Questions before Resuscitation – Neonatal Asphyxia

A
  1. Term gestation
  2. Good tone
  3. Breathing/crying
    if one answer is NO, go to initial resuscitation step
28
Q

Initial Resuscitation Steps

A
  • Warm
  • Position - Suction
  • Dry
  • Stimulate The Infant ˆ

Next
- Evaluate Respi + HR
- If apnea/gasping or HR <100bpm provide PPV with 21% O2(term), 30% O2 term
- Golden Minute (60 secs) mark for completing initial step, re-evaluating- begin ventilation (IF required)
Next
- After 30 secs of PPV
- Evaluate HR
- If HR is <100bpm, then correct PPV (Positive Pressure Ventilation)
- Reassess HR (30 sec later)
- HR less than 60 bpm? = start chest compression cooperating w/ PPV

Reassess
- After 60 secs, reassess !!!!!!
- HR greater 60bpm, stop compression, continue PPV
- 30 secs, reassess
- HR greater 100bpm and regular breathing, stop ppv

29
Q

Levels of Asthma Control

A

(photo)

30
Q

Complications of Malnutrition

A
  1. Nutritional anemia
    - Most common
    - Microcytic hypochromic anemia
  2. Vitamin deficiency
    - Fat-soluble vitamin A and D deficiency
  3. Zinc deficiency
    - Around 3⁄4 children
    - May lead to Lower immunal function
  4. Infection
    - Repeated respiratory infection
    - Pneumonia
    - UTI
    - Protactred course of disease, malnutrition worse, vicious circle forms
  5. Spontaneous hypoglycemia
    - Happens suddenly
    - Pale
    - Unconsciousness
    - Slow pulse rate
    - Apnea
    - Low temperature
    - No seizure
    - Death may happen if no injection of glucose IV w/o delay
31
Q

Diagnosis of Malnutrition

A

Consider the age and feeding history of patient
- Sign and symptoms (e.g weight loss, subcutaneous fat loss, systemic
dysfunction and nutrient deficiency)
- Regular growth monitoring and follow-up (e.g use monitoring chart)
- Height (length) and weight are basic measures for diagnosis WHO classification
- Based on SD of body weight and height
- Underweight – 2SD or less
- Moderate – 2SD to -3SD
- Severe -3SD or greater which indicates Acute/Chronic Malnutrition

32
Q

Spontaneous Hypoglycemia of Malnutrition

A
  • Happens suddenly
  • Pale
  • Unconsciousness
  • Slow pulse rate
  • Apnea
  • Low temperature
  • No seizure
  • Death may happen if no injection of glucose IV w/o delay
33
Q

Protein-Energy Malnutrition (PEM)

A
  • Disease caused by deficiency of energy and protein
  • Weight not increased or decreased
  • Wasting or edema
  • Decreased or disappeared subcutenous fat
  • Decreased function of organs
  • Often accompanied by deficiency of Multiple Micronutrients
34
Q

Rules of Growth and Development

A
  • It’s a continuous and stage-by-stage process
  • Unbalanced development of systems and organs
  • Individual differences of Growth and Development
    o Growth “track” among children are different
    o Caused by inherited potential and environmental factors
  • General principles of Growth and Development
    o Up to Down – raise head, sit, stand
    o NeartoFar–armtohand
    o Gross to fine – palm to finger
    o Elementary to senior – observe, feeling, remember analyze o Simple to complex – line, circle, whole picture
35
Q

Tuberculous Meningitis

A
  • A chronic infectious disease of CNS caused by tubercle bacillus
  • Age of onset
    o More common <3 yrs old infant and toddler
    o Within 1yr (esp 3-6 months) after Primary Tubercular Infection
  • Infant and toddler’s BBB function is not perfect, immunologic function is
    poor
  • Source of meningeal bacteria
    o Hematogenous spread when systemic miliary tuberculosis
    o Tuberculosis lesion spreading from Brain Parenchyma, Spine, Skull,
    Middle ear, and Mastoid
36
Q

Cerebrospinal Fluid Examination for diagnosis of Tuberculous Meningitis

A
  • Pressure Increased
  • Appearance – clear or round-glass appearance
  • Leukocyte count – 50-500x106/L, mainly lymphocyte, reach 70-80%
  • Protein quantitative analysis increase 1.0-3.0 g/L
  • Glucose decrease usually <0.3 g/L
  • Chloride decrease, 85.5-102.6 mmol/L (500-600 mg/dL)
  • Both reduction of glucose and chloride is a typical change of TB Meningitis
37
Q

Diagnosis of TB Meningitis

A
  • PPD test (+) in later stage false negative may appear
  • Chest X-Ray examination – 85% TB change in TB Meningitis
  • Cerebral CT or MRI scan –
    o shadow enhancement of basal ganglia, o increased density of cerebral cister,
    o calcification,
    o ventricular enlargement
    o Cerebral edema
    o Focal infarction
  • Fundus examination – miliary nodules
38
Q

Clinical Manifestation of TB Meningitis

A
  1. Early Stage (Prodromal Stage)
    - Personality change + symptoms of TB intoxication
    - Few words say, easy get tired, irritable, fever, night sweat, vomiting,
    diarrhea
    - Headache (elder children), drowsiness (infant), gaze
  2. Intermediate Stage (Meningeal Irritation Sign)
    - Mainly Meningeal Irritation Sign
    - Headache, projectile vomit, drowsiness, convulsion, neck rigidity
    - Babinski sign, Kernig sign both (+)
    - Cranial n. palsy, facial paralysis, optic papilla edema, tubercular nodus of
    choroid
    - Infant fontanel bulging
  3. Advanced Stage (Coma Stage)
    - Disturbance of Consciouss (mainly)
    - Above manifestation aggravated
    - Convulsion, coma, electrolyte disorder, cerebral hernia, death
39
Q

Treatment of TB

A
  • General treatment o Rest
    o Diet
    o Outdoor activity
    o Full duration of Treatment
    o Pay attention to Reexamination
  • Medication
    o Isoniazid
    o Rifampin
    o Streptomycin o PZA
    o Ethambutol
    o ETH
    o PAS
  • Standard therapy
    o Daily take medicine orally, therapeutic course 9-12 months
  • Therapy in stages
    o Intensive phase of Treatment 3-4 months
    o Consolidation phase of treatment 12-18 months
  • Directly Observed Therapy Sort Course (DOTS)
40
Q

ABCDE resuscitation for treatment of Asphyxia of Newborn

A
  1. A (Airway)
    - Establish open airway
    - Position of the infant (no extend/flex)
    - Suction mouth, nose
    - Suction any blood, secretion
    - Placing a guedel airway
  2. B (Breathing)
    - Initiate breathing
    - Tactile stimulation
    - PPV if necessary (+ press ventilation)
    - Mask ventilation placed over mouth and nose
  3. C (Circulation)
    - Maintain circulation
    - Stimulate cardiac compression
  4. D(Drugs)
    - Adrenaline -> low HR
    - Sodium bicarbonate acidosis
    - Naloxone bradypnea
  5. E (Evaluation)
    - Respiration – if none/gasp, give PPV 21% oxygen 15-30 sec
41
Q

Severe manifestation of AGN

A
  1. Hypertensive Encephalopathy
    - Approx 5% of hospitalized children
    - HTN usually severe, accompanied by CNS dysfunction (e.g headache, vomit,
    depressed sensorium, confusion, visual disturbances, aphasia, memory loss,
    coma, convulsion)
  2. Circulatory Congestion
    - Dyspnea, orthopnea, cough – present
    - Pulmonary Rales often audible
    - Patient with otherwise normal Cardiovascular system, Cardiac failure is
    unusual
    - Pallor is common at onset and is not explained entirely by Anemia
  3. Acute Insufficiency
    - Glomerular inflammation (e.g Cellular Prolfieration, Edema)
    - Capillary loop is narrowed
    - Glomerular Filtration reduce
42
Q

Tuberculous meningitis (character, diagnosis)

A

PPD test (+) in later stage false negative may appear
- Chest X-Ray examination – 85% TB change in TB Meningitis
- Cerebral CT or MRI scan –
o shadow enhancement of basal ganglia, o increased density of cerebral cister,
o calcification,
o ventricular enlargement
o Cerebral edema
o Focal infarction
- Fundus examination – miliary nodules

  1. Early Stage (Prodromal Stage)
    - Personality change + symptoms of TB intoxication
    - Few words say, easy get tired, irritable, fever, night sweat, vomiting,
    diarrhea
    - Headache (elder children), drowsiness (infant), gaze
  2. Intermediate Stage (Meningeal Irritation Sign)
    - Mainly Meningeal Irritation Sign
    - Headache, projectile vomit, drowsiness, convulsion, neck rigidity
    - Babinski sign, Kernig sign both (+)
    - Cranial n. palsy, facial paralysis, optic papilla edema, tubercular nodus of
    choroid
    - Infant fontanel bulging
  3. Advanced Stage (Coma Stage)
    - Disturbance of Consciouss (mainly)
    - Above manifestation aggravated
    - Convulsion, coma, electrolyte disorder, cerebral hernia, death
43
Q

Primary Complex of PPTB

A
  • Primary lesion
  • Enlarged lymph node
  • Linking lymphangitis exist at the same time
44
Q

4 deformities which compose tetralogy of fallot

A

The 4 Malformations of TOF include
o Overriding aorta
o Pulmonic stenosis
o Ventricular septal defect
o Right ventricular hypertrophy

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