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A. AMC - MCQ MATEO 2024 > Paediatrics > Flashcards

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

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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

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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

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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

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5
Q

TORCH CONGENITAL INFECTIONS

A
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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

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7
Q

NEONATAL JAUNDICE

PHYSIOLOGIC JAUNDICE
VS
PATHOLOGIC JAUNDICE

A
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8
Q

ALGORYTHIM JAUNDICE

A
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9
Q

BREASTFEEDING JAUNDICE
AND BREAST MILK

A
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10
Q

NEONATAL JAUNDICE TX

A
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11
Q

CRIGER NAJJAR SYNDROME

A
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12
Q

CAUSES INDIRECT VS INDIRECT PATHOLOGIES

A
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13
Q

DIAPHRAGMATIC HERNIA
Best image
Tx

A
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14
Q

RESPIRATORY DISTRESS SYNDROME
SYMPTOMS

A
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15
Q

RESPIRATORY DISTRESS SYNDROME
DX?

A
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16
Q

RESPIRATORY DISTRESS SYNDROME

PREVENTION?
MEDICAL TREATMENT?
COMPLICATIONS?

A
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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

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18
Q

TRANSIENT TACHYPNEA OF THE NEWBORN (TTN)

A
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19
Q

Necrotizing Enterocolitis:

A
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20
Q

Necrotizing Enterocolitis:
Symptoms
physical exam?
risk factors?

A

<35 weeks gestation

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21
Q

Necrotizing Enterocolitis:
investigations:

A
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22
Q

Necrotizing Enterocolitis:
TX

A
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23
Q

INMUNIZATION CHILDHOOD

A
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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

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25
Q

CHICKEN POX

varicella zoster (herpers virus 3)

A

Risk factors: inmunocompromised
sick contacts

causes chicken pox, shingles

fiebre, malaise

asynchronous vesicular rash head and trunk -> extremities
develops crust

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26
Q

CHICKEN POX tx:

oral antivirals:
profilaxis?
pregnant?

A
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27
Q

exclusion periods for most diseases

A
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28
Q

HAND AND FOOT MOUTH DISEASE

VIRUS?

A

**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

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29
Q

ROSEOLA INFATUM
VIRUS?

A

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)

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30
Q

ROSEOLA VS DIFERENTIALS

A
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31
Q

ORAL RASHES IMAGES

A
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32
Q

EBV
VIRUS

A

EPSTEIN BAR OR HERPES VIRUS 4

Infectious mononucleosis

symptom: fever+pharyngitis+maculopapular rash (if amoxiciliine)
lindafenopatias

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33
Q

VEB
labs
tx

A
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34
Q

RHEUMATIC FEVER

virus
pathogenesis

A
  • inmunologic reaction to streptococus A infection.
  • aboriginals top end australia (streptococcal pyoderma is the main cause)

location
mitral valve> aortic valve > tricuspide

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35
Q

rheumatic fever

presentation

A
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36
Q

rheumatic fever

investigations

A
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37
Q

Diagnosis of rheumatic fever

A
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38
Q

rheumatic fever tx

A

IM benzathine peniciline H injections 3-4 weeks for 10 years

if patient doesnt want to (oral peniciline V twice day )

allergic to fever

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39
Q

rheumatic fever investigations
+
TX

A
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40
Q

BRONCHIOITIS

A

WHEEZING
<2 YEARS

RSV
RESPIRATORY SYNCITIAL VIRUS

low grade fever

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41
Q

bronchiolitis differencials
tx

A

conservative:
hidratation
O2 if needed

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42
Q

bronchiolitis
mild/moderate/severe

A
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43
Q

EPIGLOTTITIS
ETIOLOGY?
CLINIC:

A

**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)

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44
Q

EPIGLOTTITIS
.
investigations:
tx :

A
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45
Q

CROUP

A

**PARAINFLUENZA VIRUS **
BARKING COUGH
SYMPTOMS GET WORST AT NIGHT

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46
Q

CROUP TX

A

DEXAMETHASONA ORALLY / PREDNISOLONA

SEVERE
NEBULISED ADRENALINE 5ML OF UNDILUTED ADRENALINE 1:1000+ DEXAMETHASONE

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47
Q

PERTUSIS

A

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

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48
Q

PERTUSIS INVESTIGATIONS

A

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

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49
Q

Control of diagnosed case PERTUSIS
Vaccionation?

A

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

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50
Q

Pertusis TX

A

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

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51
Q

PROFILAXIS PERTUSIS

A

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

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52
Q

Pertusis complications

A

apnea, pneumonia, cianosis, encefalopatia

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53
Q

Dysplasia of the hip
risk factors
5fs

A
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54
Q

screening DDH

A

ultrasound for high risk babies ,
ortolani and bartolini enough

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55
Q

investigations DDH

A

Barlow = aduccion y posterior = positivo se disloca- test dislocate hip

Ortolani= abeduccion y reducir a su puesto = se arregla - test reduce hip

56
Q

DHH tx

A
57
Q

Perthe disease
risk factors

A

avascular necrosis of the femoral head.

limited movement ABDUCTION IN Internal Rotation

58
Q

perthe disease
mx

A
59
Q

transient synovitis
clinical features

TX?

A

irratable hip self limiting synovial inflammation
blood test and x ray NORMAL

ULTRASOUND SHOWS FLUID IN THE JOINT

60
Q

Slipped capital femoral epiphysis:

A

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
Q

Foreign Body Aspiration:

A

normal x ray does not exclude foreign body

<4 anos

most common site right main bronchus

62
Q

Foreign Body Ingestion :

A
63
Q

Foreign Body Ingestion :

A
64
Q

inhaled body algorythim

A
65
Q

Growing pains:

A

related to trauma, excessive exercise or sports

66
Q

Innocent murmurs:

A

<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
Q

7S Of innocent murmurs

A
68
Q

Nocturnal enureis:

A

5 > older
boys affected 3 times more
family tendencis

constipation
sleep apnea
UTIS
DM
psychological problems

69
Q

Nocturnal enureis:

UROTHERAPY

A
70
Q

Nocturnal enureis:

ALARM THERAPY

A

succes is when 14 days of dry

71
Q

Nocturnal enureis:

medications

A
72
Q

HYPERTROPHIC PYLORIC STENOSIS

ePIDEMIOLOGY/ ETIOLOGY

A

ETILOGY
eritromicine

73
Q

HYPERTROPHIC PYLORIC STENOSIS

presentation

A

vomito en min a 1 hora
vomito no bilioso
proyectil
2 weeks- 2 months presentation

OLIVE SHAPED MASS

74
Q

HYPERTROPHIC PYLORIC STENOSIS

INVESTIGATIONS + tx

A

metabolic alcalosis (hipokalemia/hipocloremia)

75
Q

GI BLEEDING CHILDREN

HISTORY

A
76
Q

DIFERENCIAL BLEEDING GO

A
77
Q

swallowed maternal blood
malrotation
anorectal fisure
allergic colitis

A
78
Q

infecto=ious colitis
inflamatory bowel disease
juvenile polyps

A
79
Q

intussuception

signs and symptoms

A

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
Q

intususception TX algorithm

A
81
Q

meckels diverticulum

A
82
Q

HIRSCHPRUNG DISEASE

epidemiology

A

boys>girls
**absence of ganglion cells/enteric nervous plexus **
**

83
Q

HIRSCHPRUNG DISEASE

symptoms/ investigatin

A

FAILURRE TO PASS MECONIUM IN FIRST 48 H

84
Q

HIRSCHPRUNG DISEASE

BEST INITIAL TEST/ GOLD DX + TX

A
85
Q

DOWN SYNDROME

A

-it is the most common
- 1:25
- atrioventricular canal is the most common heart disease
- hirschprung
- duodenal atresia
- atlantoaxial inestability may be appreciated

86
Q

SD DOWN INVESTIGATIONS

A
87
Q

SD DOWN MX

A
88
Q

EDWARD SYNDROME

A

everything is small
most die in 1 year of life

89
Q

syndrome fragil X

A

all is big
mitral valve prolapse

90
Q

williams syndrome

A
91
Q

bedwith wiedemann syndrome

A
92
Q

ANGELMAN SYNDROME

A
93
Q

SUMMARY CONGENITAL SYNDROMES

A
94
Q

NOONAN SYNDROME

A

FACIES + SHORT STATURE + PULMONARY STENOSIS

TRIAD

-
REFER to genetic evaluation of cardiac status cosnider vision, hearing, clotting. status. possible epilepsy

95
Q

asthma dx ?

A

everything normal besides wheezel
SOB
episodic
worse at night and early morning
consider other causes
response to beta2 agonistas

96
Q

asthma history clinic

A
97
Q

primary investigations in preschooler age 1:5

A
98
Q

mx of asthma releiver
1:5 age

A

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
Q

mx of asthma
>6 age

A

RELIEVER +
PREVENTER
(one episode every 6 weeks, frequent intermittent asthma) , nocturnal asthma, persisten asthma)

100
Q

mx of asthma preventor
1:5 age

A

*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
Q

choice of preventer:

A

*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
Q

step up preventer and salbutamol

A

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
Q

Management of children aged 6 to 11:

A

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
Q

good control of asthma : when to cease and step down

A
105
Q

ACUTE ASTHMA

severity classification

A
  • 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
Q

Red flags for alternative diagnoses to asthma:

A

productive cough
isolated cough
paraesthesia
chest pain
clubbing

107
Q

asthma mild acute algorithm

A
108
Q

asthma moderate acute algorithm

A
109
Q

asthma severe acute algorithm

A
110
Q

CYSTIC FIBROSIS

SYMPTOMS

A
111
Q

CYSTIC FIBROSIS

GENES

A
111
Q

asthma life threatening acute algorithm

A
112
Q

CYSTIC FIBROSIS

PATHOPHYSIOLOGY:

A
113
Q

CYSTIC FIBROSIS

DX

A

HEEL PRICK TEST

INMUNOREACTIVE TRYPSIN (IRT)

113
Q

CYSTIC FIBROSIS

TX

A
114
Q

PNEUMONIA

symptoms

A

FEVER + COUGH + TACHYPNEA AT REST (retractions in younger children)

115
Q

PNEUMONIA

investigations

A
116
Q

PNEUMONIA

algo

A
117
Q

severe penicilin hypersensivity

A
118
Q

complicated pneumonia

A

*Fever–Particularly fever that persists after 48 hours of appropriate treatment of pneumonia
TachypnoeaCough
*Increased work of breathing/respiratory distress
*Pleuriticchest pain or abdominal pain

**CHEST X RAY
**

119
Q

complicated pneumonia

algo

A
120
Q

Normal development

A
121
Q

*Naming colors:
*Knowing age:
*Knowing family name:
*Speaking full sentences:

A

*Naming colors-3and5yearsofage’
*Knowing age-5years
*Knowing family name-4years
*Speaking full sentences-3and5years

122
Q

Redflags for Autism

A
123
Q

growth disorders

A

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
Q

Congenital Adrenal Hyperplasia:

A

autosomal recessive disorder

**21-hydroxylase deficiency **is the most common 90%

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
Q

Precocius puberty

A
  • 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

Note:Puberty starts with THE LARCHE (Tanner stage IIinfemales<13 years)

126
Q

Cyanotic disorders

A

*Common Cyanotic Heart Disease (5 Ts) *Tetralogyof Fallot
*Transposition of great vessels *Truncusarteriosis
*Total anomalous pulmonary venous return
*Tricuspid atresia

127
Q

Tetralogy of fallot:

4 characteristics

A

Pulmonary stenosis and infundibular stenosis (obstruction to right ventricular outflow) ——
VSD —ventricular septal defect**
**Overriding aorta (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
Q

Tetralogy of fallot:

Paroxysmal hypercyanoticattacks (tets pells:

A

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
Q

Tetralogy of fallot:

dx and tx

A

Boot shaped heart

130
Q

Faillure to thrive

A

in 80% no cause is found.
healthy infants with no concerns found on history and examination, no investigations are REQUIRED

131
Q

Faillure to thrive
if concerns are found: first line investigations

A
132
Q
A
133
Q

Jmuunjijjjjjjuujjjjjj

A

A. AMC - MCQ MATEO 2024 (16 decks)

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