Paediatrics Flashcards
1
Q
sss
TOXOPLASMOSIS
transmission -
triad-
investigations?
Tx
A
1/3 trimestre
transplacentaria
triad:
chrorioretinitis
INTRACRANIAL calcifications
hydrocephalos
jaundice/growth retardation/blueberry muffin rash
investigations: serum labs toxoplasma IgG + IgM levels
most specific PCR
tx: pyrimethamine + sulfadiazine
folic acid (prevent bone marrow supression)
high mortality
2
Q
congenital rubella
transmission:
A
rubella virus- miscarriage
transmission: placenta 1 trimester (<16 weeks 90% transmission)
prevention: measles, mumps and rubella (MMR) vaccine before pregnancy
IgG -igM pregnncy planing (if not give her 2 dosis 1 month apart)
Rubella vaccine are contraindicated in pregnancy and pregnancy should be avoided 28 days after rubella
3
Q
congenital rubella
symptoms
A
**SENSORIAL HEARING LOSS
CARDIAC: PDA
PULMONARY ARTERY STENOSIS
**
blueberry muffin rash
extramedullary hematopoiesis
cataracts/glaucoma / claudy cornea
If rubella is confirmed during first trimester of pregnancy then Offer Termination because there is a 90% chance that it can cause CRs Congenital rubella Syndrome
Multiple Features include Cataract,Deafness,Intellectual disabilities,cardiac abnormalities IUGR and inflammatory lesions on brain,lung,liver and bone marrow
4
Q
CMV
infection
symptoms=
investigations
A
transplacental 1 trimestre
90% asymptomatic
purpuric rash
microcefalia
Sensorineural hearing loss
chorioretinitis
IgG/IgM
gold standar pcr urine, saliva blood
5
Q
TORCH CONGENITAL INFECTIONS
A
6
Q
SUDDENINFANTDEATHSYNDROME/SIDS
def
dx
tx
A
Definition:sudden death at<1yearpeak 4 months of age that is unexplainable after a thorough investigation
dx = AUTOPSY IS A MUST
TX= CONSERVATIVE SUPPORT THE FAMILY
POLICE AND CORONER MUST BE NOTIFIED
7
Q
NEONATAL JAUNDICE
PHYSIOLOGIC JAUNDICE
VS
PATHOLOGIC JAUNDICE
A
8
Q
ALGORYTHIM JAUNDICE
A
9
Q
BREASTFEEDING JAUNDICE
AND BREAST MILK
A
10
Q
NEONATAL JAUNDICE TX
A
11
Q
CRIGER NAJJAR SYNDROME
A
12
Q
CAUSES INDIRECT VS INDIRECT PATHOLOGIES
A
13
Q
DIAPHRAGMATIC HERNIA
Best image
Tx
A
14
Q
RESPIRATORY DISTRESS SYNDROME
SYMPTOMS
A
15
Q
RESPIRATORY DISTRESS SYNDROME
DX?
A
16
Q
RESPIRATORY DISTRESS SYNDROME
PREVENTION?
MEDICAL TREATMENT?
COMPLICATIONS?
A
17
Q
Meconium Aspiration Syndrome:
A
Dark, greenish staining or streaking of the amniotic fluid or the obvious presence of meconium in the amniotic fluidLimpness in infant at birth
Antibiotics to treat infection
Breathing machine to keep the lungs inflatedUse of a warmer to maintain body temperature
Tapping on the chest to loosen secretionsIf there have been no signs of fetal distress during pregnancy and the baby is a vigorous full-term newborn, experts recommend against deep suctioning of the windpipe for fear of causing a certain type ofpneumonia.
The most accurate test to check for possible meconium aspiration involves looking for meconium staining on the vocal cords with a laryngoscope
18
Q
TRANSIENT TACHYPNEA OF THE NEWBORN (TTN)
A
19
Q
Necrotizing Enterocolitis:
A
20
Q
Necrotizing Enterocolitis:
Symptoms
physical exam?
risk factors?
A
<35 weeks gestation
21
Q
Necrotizing Enterocolitis:
investigations:
A
22
Q
Necrotizing Enterocolitis:
TX
A
23
Q
INMUNIZATION CHILDHOOD
A
24
Q
MEASLES
PRESENTATION
TX?
COMPLICATION
A
3 DAYS PRODROM
COUGH
CORYZA
CONJUNTIVITIS
HIGH FEVER
2-3 days-> THEN -> RASH
PHYSICAL EXAM
KOPLIK SPOTS
RASH HEAD TO NECK (EXCLUDES PALMS)
TX- SUPPORTIVE + VITAMINA A
issolation
COMPLICATION: Subacute sclerosing panencephalitis.
**suspected: **until test known
confirmed: until IG+IM-
if measles develops: at least 4 days after rash
25
CHICKEN POX
## Footnote
varicella zoster (herpers virus 3)
Risk factors: inmunocompromised
sick contacts
causes chicken pox, shingles
fiebre, malaise
**asynchronous vesicular rash** head and trunk -> extremities
develops crust
26
CHICKEN POX tx:
oral antivirals:
profilaxis?
pregnant?
27
exclusion periods for most diseases
28
HAND AND FOOT MOUTH DISEASE
## Footnote
VIRUS?
**COCKSACKIE VIRUS A (hand, foot and mouth) **
B (miocarditis, pericarditis)
risk factors: exposure to other virus, daycare, poor hygiene
LOW FEVER
child doesnt want to eat
investigations: **specific cox virus ig A**
TX
supportive care
ibuprofeno (oral ulcers pain)
hydratation
29
ROSEOLA INFATUM
VIRUS?
Human herpes virus 6!
also called exanthem subitum
risk factors: inmunosupression / trasnplant recipients
**HIGH FEVER FOR 3 DAYS**
FEVER DISSAPEAR THEN RASH BOOM
maculo papular
dura 2 dias
nagayma spots (erythematous paupels on the mucosa of soft palate and uvula)
30
ROSEOLA VS DIFERENTIALS
31
ORAL RASHES IMAGES
32
EBV
VIRUS
EPSTEIN BAR OR HERPES VIRUS 4
Infectious mononucleosis
symptom: fever+pharyngitis+maculopapular rash (if amoxiciliine)
lindafenopatias
33
VEB
labs
tx
34
RHEUMATIC FEVER
## Footnote
virus
pathogenesis
- inmunologic reaction to streptococus A infection.
- **aboriginals top end australia (streptococcal pyoderma is the main cause)**
location
mitral valve> aortic valve > tricuspide
35
rheumatic fever
## Footnote
presentation
36
rheumatic fever
## Footnote
investigations
37
Diagnosis of rheumatic fever
38
rheumatic fever tx
IM benzathine peniciline H injections 3-4 weeks for 10 years
if patient doesnt want to (oral peniciline V twice day )
allergic to fever
39
rheumatic fever investigations
+
TX
40
BRONCHIOITIS
**WHEEZING**
<2 YEARS
RSV
RESPIRATORY SYNCITIAL VIRUS
**low grade fever**
41
bronchiolitis differencials
tx
conservative:
hidratation
O2 if needed
42
bronchiolitis
mild/moderate/severe
43
EPIGLOTTITIS
ETIOLOGY?
CLINIC:
**medical emergency **
S pneumoniae
S pyogenesis
**haemophilus influenza type B**
HIGH FEVER+DROOLING+DYSPHAGIA+ MUFFLED VOICE+ RESPIRATORY RETRACTION
**SUDDEN ONSET**
PHYSICAL EXAM:
-cyanosus
**INSPIRATORY STRIDOR **
patients with neck hyperextended and chains protruding (sniffing dog position)
44
**EPIGLOTTITIS**
.
investigations:
tx :
45
CROUP
**PARAINFLUENZA VIRUS **
BARKING COUGH
SYMPTOMS GET WORST AT NIGHT
46
CROUP TX
DEXAMETHASONA ORALLY / PREDNISOLONA
SEVERE
**NEBULISED ADRENALINE 5ML OF UNDILUTED ADRENALINE 1:1000**+ DEXAMETHASONE
47
PERTUSIS
Bordetella pertusis
IP 7 prior cough and -21 cough
**paroxysmal cough with inspiratory whoop without FEVER mostly**
1 week = CATARRAL FASE
2-3 week = paroxysmal fase
Infants less than 6 months of age are at greatest risk of complications (apnoea, severe pneumonia, encephalopathy) and are most commonly infected by spread from family members
48
PERTUSIS INVESTIGATIONS
Laboratory confirmation is not necessary for diagnosis, but may be helpful for infection control
A nasopharyngeal aspirate/swab for PCR is the investigation of choice. The test is usually negative after 21 days, or 5-7 days after effective antibiotic therapy has been commenced
49
Control of diagnosed case PERTUSIS
Vaccionation?
Exclude from school and presence of others outside the home (especially infants and young children) until received 5 days of therapy, or coughing for more than 21 days
Unimmunised or partially immunised children diagnosed with pertussis should still complete the pertussis immunisation schedule
50
Pertusis TX
**Antibiotics**
**Consider antibiotics if:**
Diagnosed in catarrhal or early paroxysmal phase (may reduce severity)
Cough for less than 14 days (may reduce spread; reduces school exclusion period)
Admitted to hospital
Complications (pneumonia, cyanosis, apnoea)
Antibiotic options:
**Neonates**:
**Azithromycin** 10 mg/kg oral daily for 5 days
Children who cannot swallow tablets:
**Clarithromycin** liquid 7.5 mg/kg/dose (max 500 mg) oral BD for 7 days
Children who can swallow tablets:
**Azithromycin** (for children = 6 months old): 10 mg/kg (max 500 mg) oral on day 1, then 5 mg/kg (max 250 mg) daily for 4 days
If macrolides are contraindicated:
**Trimethoprim-sulphamethoxazole** (8-40 mg per mL)
0.5 mL/kg (max 20 mL) BD for 7 days
51
PROFILAXIS PERTUSIS
Prophylaxis is aimed at preventing spread to infants <6 months
There is little evidence that antibiotics prevent transmission outside of household settings, and side effects (especially gastrointestinal) are relatively common
Transmission requires close contact (exposure within 1 metre for more than 1 hour) but can be less for young infants
Most school-aged children who are fully vaccinated and do not have symptoms do not require prophylaxis
Management of immunodeficient contacts should be made on a case by case basis
Management of outbreaks may differ from below and will be conducted by DHS
52
Pertusis complications
apnea, pneumonia, cianosis, encefalopatia
53
Dysplasia of the hip
risk factors
5fs
54
screening DDH
ultrasound for high risk babies ,
ortolani and bartolini enough
55
investigations DDH
Barlow = aduccion y posterior = positivo se disloca- test dislocate hip
Ortolani= abeduccion y reducir a su puesto = se arregla - test reduce hip
56
DHH tx
57
Perthe disease
risk factors
avascular necrosis of the femoral head.
**limited movement ABDUCTION IN Internal Rotation**
58
perthe disease
mx
59
transient synovitis
clinical features
TX?
**irratable hip** self limiting synovial inflammation
blood test and x ray NORMAL
**ULTRASOUND SHOWS FLUID IN THE JOINT**
60
Slipped capital femoral epiphysis:
develop avascular necrosis despite expert treatment.
10-15 years **obese**
**Hip rotating external rotation on flexion and often lies in external rotation**
**X RAYS (ap and frog view) of BOTH HIPS**
Graded from I - IV
61
Foreign Body Aspiration:
normal x ray does not exclude foreign body
<4 anos
most common site right main bronchus
62
Foreign Body Ingestion :
63
Foreign Body Ingestion :
64
inhaled body algorythim
65
Growing pains:
related to trauma, excessive exercise or sports
66
Innocent murmurs:
<12 months **REFFER **
children over 12 months if the following 4 criteria are met:
- no abnormal physical findings
- asyntomatic (no cough, dyspnoea, palpitations, fatigue)
- no risk factors (family history, maternal gestation DM/alcohol, abuse, previous kawasaki, prematurity)
TX
REASSURANCE
REFER TO ECHOCARDIOGRAPHY IF NOT SURE
67
7S Of innocent murmurs
68
Nocturnal enureis:
5 > older
**boys affected 3 times more
family tendencis**
constipation
sleep apnea
UTIS
DM
psychological problems
69
Nocturnal enureis:
## Footnote
UROTHERAPY
70
Nocturnal enureis:
## Footnote
ALARM THERAPY
succes is when 14 days of dry
71
Nocturnal enureis:
## Footnote
medications
72
HYPERTROPHIC PYLORIC STENOSIS
## Footnote
ePIDEMIOLOGY/ ETIOLOGY
ETILOGY
**eritromicine**
73
HYPERTROPHIC PYLORIC STENOSIS
## Footnote
presentation
**vomito en min a 1 hora**
vomito no bilioso
proyectil
2 weeks- 2 months presentation
**OLIVE SHAPED MASS**
74
HYPERTROPHIC PYLORIC STENOSIS
## Footnote
INVESTIGATIONS + tx
**metabolic alcalosis (hipokalemia/hipocloremia)**
75
GI BLEEDING CHILDREN
## Footnote
HISTORY
76
DIFERENCIAL BLEEDING GO
77
swallowed maternal blood
malrotation
anorectal fisure
allergic colitis
78
infecto=ious colitis
inflamatory bowel disease
juvenile polyps
79
intussuception
## Footnote
signs and symptoms
**INTERMITTENT PAIN OR DISTRESS**
****riks factors :****
Investigations:
ultrasound (not used to excluded)
X ray (only in signs of obstruction or perforation)
**CONTRAST ENEMA / DX AND TX**
80
intususception TX algorithm
81
meckels diverticulum
82
HIRSCHPRUNG DISEASE
## Footnote
epidemiology
boys>girls
**absence of ganglion cells/enteric nervous plexus **
****
83
HIRSCHPRUNG DISEASE
## Footnote
symptoms/ investigatin
**FAILURRE TO PASS MECONIUM IN FIRST 48 H**
84
HIRSCHPRUNG DISEASE
## Footnote
BEST INITIAL TEST/ GOLD DX + TX
85
DOWN SYNDROME
-it is the most common
- 1:25
- **atrioventricular canal is the most common heart disease**
- hirschprung
- duodenal atresia
- **atlantoaxial inestability may be appreciated**
86
SD DOWN INVESTIGATIONS
87
SD DOWN MX
88
EDWARD SYNDROME
everything is small
most die in 1 year of life
89
syndrome fragil X
all is big
**mitral valve prolapse**
90
williams syndrome
91
bedwith wiedemann syndrome
92
ANGELMAN SYNDROME
93
SUMMARY CONGENITAL SYNDROMES
94
NOONAN SYNDROME
FACIES + SHORT STATURE + PULMONARY STENOSIS
=
TRIAD
-
REFER to genetic evaluation of cardiac status cosnider vision, hearing, clotting. status. possible epilepsy
95
asthma dx ?
everything normal besides wheezel
SOB
**episodic**
**worse at night and early morning**
consider other causes
response to beta2 agonistas
96
asthma history clinic
97
primary investigations in preschooler age 1:5
98
mx of asthma releiver
1:5 age
1-2 = ** 2 puffs pressurised metered dose inhaler plus spacer and facemask**
3-5 years: **2-4 puffs pressurised metered dose inhaler plus spacer**
(with facemask if unable to adecuate seal)
99
mx of asthma
>6 age
**RELIEVER +
PREVENTER**
(one episode every 6 weeks, frequent intermittent asthma) , nocturnal asthma, persisten asthma)
100
mx of asthma preventor
1:5 age
*Mild symptoms managed with salbutamol should not be given preventors unless symptoms happen atleast once per week or every 3 to 4 weeks.
***Moderate–severeflare-ups**
*(requireEDcare/oral corticosteroids) Indicated
***Life-threateningflare-ups**
*(require hospitalisationor PICU)Indicated
For children aged 2 years and older with frequent symptoms (e.g. wheeze, cough or breathlessness at least once per week) or a history of severeflare-ups(e.g. requiring emergency department visits or oral corticosteroids), consider a treatment trial of regularpreventerwith either of:
*montelukast
*an inhaled corticosteroid (low dose)
101
choice of preventer:
*When starting preventer for the first time for a child aged 2 years or over, the choice of agent can be guided by the following considerations.
*Montelukast might be considered as alternative to an inhaled corticosteroid when any of the following apply:
*The child is unable or refuses to use to MDI+ spacer/mask.
*The child has significant allergic rhinitis that requires treatment.
*Parents, despite education about risks and benefits, decline inhaled corticosteroids or are significantly concerned about their adverse effects (poor adherence is likely in this context).
102
step up preventer and salbutamol
**Step 1: SABA only **
*Can use SABA only, without regular preventer, in children who have–not required treatment for exacerbations (systemic corticosteroid or hospital presentation) in the past 12 months–symptoms occur infrequently –no other contributing factors (smoking in household, obesity, social risk factors etc)
*Most other children require maintenance treatment (preventer)
--------------------------
***Step 2: Low dose ICS via spacer (and reliever as needed)**
***Ciclesonide 80 microgonce daily or Fluticasone 50 microg twice daily**–ciclesonide has the advantages of daily dosing, lower side effect profile, PBS subsidised so lower out of pocket costs (NB not all spacer devices are compatible)
*Montelukastoral tablet
*Montelukastcan be used as an alternative first line preventer (or adjunct to ICS) in children requiring further control
*Montelukast 5 mg once daily–consider using as ICS alternative if significant parental concern regarding steroids or in children where use of MDI + spacer is particularly difficult–1 in 6 children may develop side effects with this medication including agitation, sleep disturbance and altered mood. If this occurs, cease medication to see if symptoms resolve
-----------------------------------
***Step 3: Moderate dose ICS OR low dose ICS + montelukast OR ICS/LABA (and reliever as needed)**
*Moderate dose ICS = fluticasone100 microgtwice daily or ciclesonide160microgonce daily
*ICS/LABA = budesonide/formoterolMDI 100 microg/3 microg, 2 puffs twice daily or DPI 200 microg/6 microg, one inhalation twice daily
** *Step 4: moderate dose ICS + montelukast OR ICS/LABA + montelukast OR consider referring for expert advice**.
103
Management of children aged 6 to 11:
***Reliever treatment**
***SABA (salbutamol)**: all children should be prescribed SABA with spacer, and encouraged to have inhaler and spacer with them at all times Dose: salbutamol100 microgMDI,** 6 -12 puffs (via spacer +/-mask)**
*Check number of canisters used between each review (>3 a year is high risk)
*Encourage dose-tracking (egcheck dose counter if available) to ensure canisters aren’t prematurely discarded (environmental hazard) nor used once empty
104
good control of asthma : when to cease and step down
105
ACUTE ASTHMA
## Footnote
severity classification
* If unsure if a child has anaphylaxis or asthma, treat for anaphylaxis. Treatment of both is time critical
* Metered dose inhalers (MDI) are preferable to nebulisers given their rapid delivery, comparable efficacy and fewer side effects
* Short acting beta agonist (SABA) therapy is crucial to the management of asthma
* Give steroids early in moderate, severe and life-threatening asthma
* Adolescents on combination reliever/preventer therapy (ie budesonide/formoterol dry powder inhalation) should be managed with salbutamol for an acute exacerbation requiring treatment in hospital
**The best measures of severity are general appearance, mental state, activity and work of breathing (respiratory rate, accessory muscle use, retraction)**
106
Red flags for alternative diagnoses to asthma:
productive cough
isolated cough
paraesthesia
chest pain
clubbing
107
asthma mild acute algorithm
108
asthma moderate acute algorithm
109
asthma severe acute algorithm
110
CYSTIC FIBROSIS
## Footnote
SYMPTOMS
111
CYSTIC FIBROSIS
## Footnote
GENES
111
asthma life threatening acute algorithm
112
CYSTIC FIBROSIS
## Footnote
PATHOPHYSIOLOGY:
113
CYSTIC FIBROSIS
## Footnote
DX
HEEL PRICK TEST
INMUNOREACTIVE TRYPSIN (IRT)
113
CYSTIC FIBROSIS
## Footnote
TX
114
**PNEUMONIA**
## Footnote
symptoms
FEVER + COUGH + TACHYPNEA AT REST (retractions in younger children)
115
PNEUMONIA
## Footnote
investigations
116
PNEUMONIA
## Footnote
algo
117
severe penicilin hypersensivity
118
complicated pneumonia
*Fever–Particularly fever that persists after 48 hours of appropriate treatment of pneumonia
*Tachypnoea*Cough
*Increased work of breathing/respiratory distress
*Pleuriticchest pain or abdominal pain
**CHEST X RAY
**
119
complicated pneumonia
## Footnote
algo
120
Normal development
121
*Naming colors:
*Knowing age:
*Knowing family name:
*Speaking full sentences:
*Naming colors-3and5yearsofage'
*Knowing age-5years
*Knowing family name-4years
*Speaking full sentences-3and5years
122
Redflags for Autism
123
growth disorders
**Constitutional growth delay**—child is short prior to onset of delayed adolescent growth spurt; parents are of normal height; normal final adult height is reached; growth spurt and puberty are delayed; bone age delayed compared to chronological age.
***Familial short stature—**patient is parallel to growth curve; strong family history of short stature; chronologic age equals bone age.
***Pathologic short stature**—patient may start out in normal range but then starts crossing growth percentiles. Differential diagnosis: craniopharyngioma, hypothyroidism, hypopituitarism, nutritional problems, and other chronic illnesses
**Tall Stature:**
*Usually a normal variant (familial tall stature)
*Other causes—**exogenous obesity, endocrine causes** (growth hormone excess [gigantism, acromegaly], androgen excess [tall as children, short as adults) Syndromes—homocystinuria, Sotos, Klinefelter
124
Congenital Adrenal Hyperplasia:
autosomal recessive disorder
**21-hydroxylase deficiency **is the most common 90%
Glucocorticoid and mineralocorticoid replacement are the mainstays of treatment
-
21-hydroxylase deficiency
- Decreased production of cortisol leads to increased ACTH production from pituitary gland that in turn leads to adrenal hyperplasia
- Precursor steroids **(17-OH progesterone**) **accumulates** in the blood because it can’t be converted to cortisol due to the defieciency of 21 –Hydroxylase enzyme so its shunted to androgen synthesis
Findings (with salt losing type):Due to defieciency of aldosterone along with cortisol:*Progressive weight loss (through 2 weeks of age), *anorexia,*vomiting, *dehydration Weakness, hypotension **Hypoglycemia,*hyponatremia,*hyperkalemia** *Affected females—masculinized external genitalia (internal organs normal at birth.late virilization)
INVESTIGATIONS:
low serum sodium
low glucose
high POTASSIUM
acidosis
low cortisol
increased androstenedione and testosterone
increased plasma renin and LOW ALDOSTERONE
**DEFINITE TESTE - 17-OH progesterone before and after IV ACTH**
TX
hydrocortisona
fludrocortsisone if salt losing
125
Precocius puberty
* breast development at age <8years in a girl or testicular enlargement ≥4ml at age <9years in a boy
-It may be idiopathic, genetic or secondary to intracranial lesions, with intracranial pathology more common in males and those presenting at younger age
**initial work up**
Thyroid function tests, FSH, LH and testosterone/oestradiol
*Bone age X-ray
*Gonadotropin Releasing hormone test: Stimulation test: After an intravenous bolus of GNRH there will be a brisk rise in luteinizing hormone.
*Brain MRI
***Treatment:To stop the epiphyseal fusion Give leuprolide**
## Footnote
**Note:Puberty starts with THE LARCHE (Tanner stage IIinfemales<13 years)**
126
Cyanotic disorders
*Common Cyanotic Heart Disease (5 Ts) *Tetralogyof Fallot
*Transposition of great vessels *Truncusarteriosis
*Total anomalous pulmonary venous return
*Tricuspid atresia
127
Tetralogy of fallot:
## Footnote
4 characteristics
**Pulmonary stenosis and infundibular stenosis** (obstruction to right ventricular outflow) ——
***VSD —ventricular septal defect**
***Overriding aort**a (overrides the VSD) —
***Right ventricular hypertrophy**
*Most common cyanotic lesion **Pulmonary stenosis **plus hypertrophy of subpulmonic muscle (crista supraventricularis) → varying degrees of right ventricular outflow obstruction Blood shunted right-to-left across the VSD with varying degrees of arterial desaturation and cyanosis
128
Tetralogy of fallot:
## Footnote
Paroxysmal hypercyanoticattacks (tets pells:
Acute onset of breathlessness and restlessness → increased cyanosis → gasping → syncope (increased infundibular obstruction with further right-to-left shunting
Treatment—**place in lateral knee-chest position, give oxygen, subcutaneous morphine, give beta-blockers .**
129
Tetralogy of fallot:
## Footnote
dx and tx
Boot shaped heart
130
Faillure to thrive
in 80% no cause is found.
**healthy infants with no concerns found on history and examination, no investigations are REQUIRED**
131
Faillure to thrive
if concerns are found: first line investigations
132
133
Jmuunjijjjjjjuujjjjjj
