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Year 4 PAEDS > Conditions 1 > Flashcards

Conditions 1 Flashcards

1
Q

Explain the difference between:
a) Indirect
b) Direct
hernias?

A

a) Indirect: sac passes through internal inguinal ring + along inguinal canal.
b) Direct: rare, usually prem baby/ CT disorder

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2
Q

How do you manage a hydrocele?

A

(can pinch above swelling, which can’t do w/hernia due to bowel)
Resolves with time (not emergency). Usually from newborn should resolve by 4yrs- if not then Patent Processus Vaginalus + needs op.

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3
Q

What is the key feature on USS of intussusception?

A

Target sign.

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4
Q

Classic presentation of pyloric stenosis?

A

1st born male children, ~6wks old.
Non-bilious (milky) projectile vomiting.
Poor/no wt gain, always hungry.

Hypochloraemic, hypokalaemia, hyponatraemic alkalosis!!!

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5
Q

What are the radiological features of Necrotizing Enterocolitis (NEC)?

A

Pneumatosis (gas in bowel wall). Bowel loops on Xray.

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6
Q

What does Malrotation with Volvulus show as on upper GI contrast?

A

DJ flexure to R of midline, corkscrew appearance of jejunum.

DJ should be to the left of vertical line + level w/ the gastric outlet

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7
Q

What is an Exomphalos?

A

Presence of abdominal contents in sac at umbilicus. Covered w/ membrannes.
A/w chromosomal anomalies.

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8
Q

What is Gastroschisis?

A

Abdominal contents through defect to right of umbilical cicatrix (not covered w/membrane).
No real associated anomalies (unlike exomphalos)

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9
Q

Causes of Bronchiolitis?

A

RSV (90%)
Rhinovirus
Adenovirus
Parainfluenza

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10
Q

Presentation of Bronchiolitis?

A
  • Start w/coryza
  • Wheeze, fine end-inspiratory crackles + dry cough
  • Signs of respiratory distress
  • Apnoea in <4months (serious)
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11
Q

Investigations for Bronchiolitis?

A
  • Examination: overexpansion of chest, wheeze + creps, nasal flaring.
  • Pulse oximetry
  • Nasal swabs (PCR to identify RSV)
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12
Q

How is most bronchiolitis managed? (+ what prophylactics for high-risk groups?)

A
  • At home, usually self-limiting (peak of illness: 3-5days)

- Prophylactic Palivizumab against RSV

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13
Q

When would you admit a child for Bronchiolitis?

A
  • Apnoea
  • Child appears seriously unwell
  • Central cyanosis
  • Severe resp distress
  • Difficulty feeding (<50% feeds)
  • Clinical dehydration
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14
Q

What is the supportive management for Bronchiolitis?

A
  • Humidified O2 by nasal cannula
  • NO bronchodilators (dont do anything)
  • Consider maintenance fluids
  • Consider CPAP if hypercapnia
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15
Q

What is Croup? (larngotracheobronchitis)

A
  • Inflammation + ^secretions of the larynx, trachea + bronchi.
  • Oedema in the subglottic area, v dangerous as can obstruct airway.
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16
Q

What are some causes of Croup?

A

(viral!)

  • Parainfluenza (most common)
  • Humanmetapneumovirus
  • RSV
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17
Q

Presentation of Croup?

A

(often starts + worse at night)

  • 6months-6yrs
  • Coryzal prodrome
  • Initial sx in larynx (stridor), then trachea/bronchi (barking cough + wheeze)
  • Severe deterioration often accompanied by reduction in the stridulous noise.
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18
Q

Management of moderate-severe croup?

A
  • Inhalation of warm air (no proven benefit but widely used)
  • Inhaled salbutamol/budesonide
  • Oral dexameth/ pred
  • If severe obstruction = nebs adrenaline /oxygen given via facemask.
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19
Q

What is Bacterial tracheitis? (pseudomembranous croup)

A

Rare but dangerous.
Caused by: Staph. aureus.

Similar to severe viral croup except: ^fever, rapidly progressive airway obstruction w/ copious thick secretions.

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20
Q

What is Epiglottitis caused by?

A

Haemophilus influenzae Type B

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21
Q

How does Epiglottitis present?

A
  • Affects 2-7yrs
  • Child presents acutely w/signs of toxicity, fever, DROOLing, unable to swallow.
  • Soft inspiratory stridor, not hoarse, rarely coughs.
  • A/w sepsis
  • Characteristic posture, sit upright w/chin thrust forward.
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22
Q

Management of Epiglottitis?

A
  • Do NOT examine mouth/airway. Do NOT assess child lying down.
  • Intubation (under GA)
  • IV Cefuroxime/ Ceftriaxone or ampicillin
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23
Q

What prophylaxis should be offered to all household contacts of Epiglottitis?

A

Rifampicin

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24
Q

What is Transcient Early Wheezing?

A

Wheeze a/w immune response from viral infection (bronchiolitis), in most pre-schoolers.
Usually episodic. Often a/w coryzal sx/
Usually fully resolved by 5yrs, when ^airway size.
(vs persistent + recurrent wheezing)

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25
Q

Pathophysiology of asthma?

A
  • Bronchial Inflam: oedema, ^mucus production, infiltration w/cells (eosinophils, mast cells, neutrophils, lymphocytes)
  • Bronchial hyperresponsiveness
  • Airway narrowing: reversible airflow obstruction (e.g. peak flow variability)
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26
Q

Organisms causing Pneumonia in:

a) Neonates
b) Infants
c) >5yrs

A

a) -Group B beta-haem strep (ONLY newborn)
- Gram -ve enterococci
b) (^likely virus)
- RSV
- Strep pneumoniae
- Haemophilus influenzae
- Bordatella pertussis
- Chlamydia trachomatis
c) (^likely bacterial)
- Mycoplasma pneumoniae (more insidious onset)
- Strep pneumoniae
- Chlamydia pneumoniae

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27
Q

What may a respiratory exam show in a child with pneumonia?

A
  • End-inspiratory coarse creps.

- Classic signs of consolidation w/dullness to percussion often absent in young children

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28
Q

Management of pneumonia?

a) Acutely ill
b) Less ill/ older children
c) Newborn
d) If suspect mycoplasma

A

a) IV penicillin
b) Amoxycillin PO
c) Co-amox
d) Macrolide (erythromycin)

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29
Q

Causes of the common cold? (coryza)

A
  • Rhinovirus, RSV.

- Mx: self limiting. Best treated w/Calpol or Ibuprofen.

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30
Q

Causes of Tonsillitis/ Pharyngitis?

A

-Group A Strep (biggest cause in children), adenovirus, enterovirus, EBV.

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31
Q

Treatment for Tonsillitis/ Pharyngitis?

A

Phenoxymethypenicillin (Pen-V), or erythromycin.

avoid amoxicillin > causes widespread macpap rash if infection caused by EBV

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32
Q

What is the mutant gene for CF , + what does this gene code for?

A
  • Delta F508
  • Codes for a protein which controls Na+ and Cl- transport across the membrane of secretory epithelial cells.

(leads to a higher salt content of sweat + thicker secretions)

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33
Q

What are 4 key complications of CF?

A
  • Lungs: small airway obstruction, ^ infections.
  • Pancreas: ducts obstructed > fibrosis.
  • Biliary cirrhosis: poor lipid absorption.
  • Vans deferens obstruction: infertility in males.
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34
Q

Presentation of CF?

A
  • Recurrent chest infections
  • Inefficiency of gaseous exchange (dyspnoea, chronic cough, hyperinflated chest)
  • Meconium ileus
  • Malabsorption + malnutrition (blockage of pancreatic duct)
  • Steatorrhoea (pancreatic insufficiency- low elastase in faeces)
  • Finger clubbing
  • Reproductive tract failure
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35
Q

What may a chest Xray of CF show?

A
  • Hyperinflation
  • Bronchial thickening
  • Upper lobe bronchiectasis
  • Central lines
  • ?Infection
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36
Q

What investigations are there for CF?

A
  • Newborn heel-prick test (Guthrie test)- for immunoreactive trypsinogen (IRT)
  • Sweat test (chloride conc: 60-125mmol/L)
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37
Q

Management of CF?

A
  • Kaftrio: Symkevi (ivacaftor + tezacaftor) + elexacaftor.
  • Recurrent chest infections: prophylactic Fluclox (usually via PICC line)
  • Neb bronchodilators + steroids for nasal polyps.
  • Nutritional mx (vit A, E, D, K).
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38
Q

What is used to measure disease progression in CF?

A

The FEV1 is an indicator of clinical severity + declines w/ disease progression.

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39
Q

What is the commonest late complication of CF?

A

DM

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40
Q

Why are middle ear infections more common in 6-12months?

A

Their eustachian tubes are shorter, horizontal + functionally poorer.

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41
Q

Common pathogens for acute OM?

A

RSV, rhinovirus, pneumococcus, HiB

42
Q

Signs of acute OM?

A

Tympanic membrane is bright + red + bulging, loss of normal light reflection.
Potential perforation of ear drum, pus in ear canal.

43
Q

Management of acute OM?

A
  • Treat pain/fever w/ paracetamol + ibuprofen.
  • Amoxicillin 5-7days can be given, but most cases resolve spontaneously.
  • Abx shorten duration of pain, don’t reduce hearing loss.
44
Q

Complications of Acute OM?

A
  • Repeat OM can lead to OM w/effusion (GLUE EAR!)= most common cause of conductive hearing loss in children!
  • Meningitis/Mastoiditis
45
Q

Presentation of OME/GLue Ear/Serous OM?

A
  • Common in 2-7yrs
  • Asymptomatic apart from hearing loss (confirmed by tympanic hearing loss on a hearing test)
  • Ear drum dull + retracted
46
Q

Management of Glue ear?

A
  • Usually resolve spontaneously

- Grommets (effusion drained)

47
Q

Prevention of TB in high risk children?

A

BCG offered at birth to high risk.

DO NOT give BCG to HIV/immunosuppressed children due to risk of dissemination.

48
Q

What are the systemic sx of TB? (when the bacilli is nolonger contained to the lungs + is circulating the body by lymphatics)

A
  • Fever
  • Wt loss
  • Haemoptysis/cough
  • Lymphadenopathy + lung lesions (constitutes the ‘Ghon complex’)
49
Q

Investigations for TB?

A
  • Mantoux test (falsely +ve due to past vaccinations- like BCG)
  • CXR
  • Sputum sample
  • Ineterferon-gamma release assay (IGRA)
  • ALWAYS test for HIV too (and vice versa for TB if have HIV)
50
Q

Characteristic appearance of TB on a CXR?

A
  • Calcified masses
  • Enlargement of peri-bronchial lymph nodes
  • Collapse + consolidation in affected lungs
  • Pleural effusions
51
Q

Treatment for TB? (+ what if they are during/after puberty?)

A
  • Triple/Quadruple therapy: Rifampicin + Isoniazid + Pyrainamide + Ethambutol.
  • After 2months: (reduce) Rifampicin + Isoniazid.
  • Treatment duration is 6 months!
  • If in/after puberty: add Pyridoxine!! (prevents peripheral neuropathy, complication of isoniazid)
52
Q

Presentation of Whooping Cough?

A
  • 1wk coryzal sx (catarrhal phase)
  • 3-6wks of characteristic paroxysmal cough, followed by inspiratory whoop (paroxysmal phase)
  • During a paroxysm- child goes red/blue in face + mucus flows.
  • Sx gradually decrease (covalescent phase), but may last months
53
Q

How may whooping cough present differently in infants?

A

-Cough may be absent + apnoea is a feature

54
Q

Treatment for Whooping COugh?

A
  • Erythromycin (only eradicates organism in catarrhal phase- but nearly always given anyway)
  • Close contacts= erythromycin prophylaxis
55
Q

What is neuropathic bladder? (a cause of enuresis in children)

A
  • Bladder is enlarged + irregular thick walls. Fails to empty properly, distended on presentation.
  • Associated w/ Spina Bifida
  • Sometimes abnormal perineal sensation, anal tone, sensory loss in S2/3/4
56
Q

What are some causes of secondary enuresis?

A
  • Emotional onset (commenest)
  • UTI
  • Polyuria from osmotic diuresis in diabetes
57
Q

Investigations for enuresis?

A
  • Urine sample
  • Consider a KUB USS (structural abnormalities?)
  • Urodynamic studies
  • Xray spine (vertebral abnormality)
  • MRI: non-bony spinal defect e.g. tethering of the cord.
58
Q

What is the definition of nocturnal enuresis?

A

Involuntary voiding of urine during sleep.
At least 2x/week.
Age >5yrs

59
Q

Causes of Nocturnal Enuresis?

A
  • Emotional (nearly always)
  • UTI
  • Severe faecal impaction
  • DM
  • Genetic link w/ delayed development of sphincter control
60
Q

‘3 systems approach’ for nocturnal enuresis?

A
  1. (1st choice) Ability to wake to full bladder sensation (alarm!! Operant conditioning)
  2. Adequate functional bladder capacity (&daytime fluid, regulate toileting + ?oxybutynin which helps overactive bladder)
  3. Arginine vasopressin (desmopressin)

++++ Psychological wellbeing !!!

61
Q

What is Desmopressin?

A

Drug for enuresis (for short term).

DONT use desmopressin spray in kids due to hyponatraemic s/e.

62
Q

What are some other drugs for Enuresis?

A
  • Imipramine (2nd line)- more s/e, concern of toxicity.

- Oxybutinin: for detrusor instability (daytime freq + wetting)

63
Q

What organisms are responsible for UTI in children? (gram -ve)

A
  • E coli (90% of ALL)
  • Klebsiella
  • Proteus (more common in boys, predisposes to formation of phosphate stones)
64
Q

Organisms responsible for UTI in children? (gram +ve)

A

Staph saprophyticus
Enterococcus
Staph aureus
Pseudomonas- may indicate structural abnormality in UT affecting drainage.

65
Q

Are UTIs more common in boys or girls?

A
  • Neonatal period: boys>girls becuase posterior urethral valve more common in boy.
  • > 1yrs: girls 3x more common
66
Q

Red Flags of UTI in childhood?

A
  • Fever <3months (temp would be sepsis until proven otherwise!!)
  • Flank pain
  • Irritable/floppy
  • HTN (chronic kidney problem?)
67
Q

Presentation of UTI in:

a) Neonate
b) Infants
c) Older

A

a) prolonged jaundice, apnoea, wt loss, collapse.
b) fever, irritable, D+V, failure to thrive, offensive urine, febrile convulsions (>6months)
c) More specific sx: dysuria, freq, loin/abdo pain, fever, lethargy + anorexia, offensive/cloudy urine, recurrence of enuresis.

68
Q

Investigations for UTI?

A
  • Urine sample (older: midstream. infants: ‘clean catch’)
  • Look for other sources of infection
  • Dipstick: Nitrates can have false -ves. Leucocyte +ve.
69
Q

What is an Atypical UTI?

A
  • Septic
  • Poor urine flow
  • Abdo mass
  • ^creatinine
  • Slow response to treatment
  • Not E. coli
  • Recurrent UTI
  • MALE !!!!
70
Q

How do you investigate an Atypical UTI?

A
  • Renal USS (ALL <6months)
  • DMSA radioisotope scan (for signs of renal scarring, do after active infection)
  • MCUG (micturating cystourethrogram) indicated if <1yrs for bladder new outflow + VUR.
71
Q

Interpretation of results in UTI:

a) Leucocyte esterase & nitrate +ve
b) Leucocyte esterase -ve & nitrate +ve
c) Leucocyte esterase +ve & nitrite -ve

A

a) Regard as UTI
b) Start abx treatment (diagnosis depends on urine culture)
c) Start abx treatment only if clinical evidence of UTI.

Nitrite: good indicator of UTI.
Leucocyte esterase: also positive in febrile illness, balanitis + vulvovaginitis.

72
Q

Management of UTI? (no sepsis)

A
  • Simple UTI: Trimethoprim 7days

- USS for UTI if <6months/ atypical/ recurrent.

73
Q

Management of UTI in sepsis? (in very young, treat as if for sepsis)

A
  • Broad spec 48hrs IV

- Oral switch to 7 day course

74
Q

What 3 examinations are carried out in a child presenting with Haematuria?

A
  1. Blood Pressure. (HTN= renal malfunction –> admit)
  2. Oedema (peri-orbital + ankles = glomerulonephritis)
  3. Renal mass (hydronephrosis, polycystic kidneys or tumour)
75
Q

What investigations would you carry out for potential Glomerular Haematuria?

A
  • ESR, complement levels, anti-DNA abs.
  • ASO titre + throat culture (recent strep infection precedes acute glomerulonephritis)
  • Serum creatinine, U&Es
  • Abdo/pelvic ISS
  • Renal biopsy if indicated
76
Q

What is the triad of Haemolytic Uremic Syndrome (HUS)?

A
  1. Acute renal failure
  2. Microangiopathic haemolytic anaemia
  3. Thrombocytopenia
77
Q

What is the typical prodrome for HUS?

A

-Typical HUS is secondary to GI infection with verocytotoxin-producing E.coli 0157
(so prodrome of bloody diarrhoea, which results in microangiopathic haemolytic anaemia)

78
Q

What are the causes of Glomerulonephritis in childgood?

A

Post-infectious (streptococcus) – commonest cause in childhood.
Vasculitis – Henloch-Schonlein purpura, SLE, polyarteritis nodosa.
IgA nephropathy + mesangiocapillary glomerulonephritis.
Anti-glomerular basement membrane disease (Goodpasture syndrome)

79
Q

Presentation of Glomerulonephritis?

A

Haematuria + proteinuria classically appears 1-2wks after throat/skin infection.
Oedema
Mild oliguria only- in most children!!

Otherwise ASx (w/ slight malaise, headache + loin discomfort)

80
Q

What is the difference between Transient + Persistent Proteinuria?

A

Transient- may occur during febrile illness/ after exercise. Doesn’t need Ix.
Persistent- significant, measure urine protein/creatinine ratio in early morning.

81
Q

What can Nephrotic syndrome be secondary to?

A
  • Henoch-Schonlein purpura (HSP)
  • SLE
  • Infections (malaria)
  • Allergens (bee sting)
82
Q

Investigations of Nephrotic syndrome?

A
  • Urine protein + culture
  • FBC + ESR + U&Es + Creatinine + Albumin
  • Complement levels (C3&4)
  • Antistreptolysin O / anti-DNAase titres + throat swab
  • Hep B/C screen
  • Malaria screen if travelled abroad.
83
Q

Management of Nephrotic syndrome?

A
  • Oral corticosteroids (pred), reducing dose after 4wks.

- If no response = renal biopsy (fusion of podocytes –> named minimal change disease)

84
Q

What are the features suggestive of steroid-sensitive nephrotic syndrome?

A
  • 1 to 10yrs
  • No macroscopic haematuria
  • Normal BP/ complement levels/ renal function
85
Q

Complications of Nephrotic Syndrome?

A
  • Hypovolaemia: peripheral vasoconstriction + urinary sodium retention. Requires urgent mx w/ IV albumin.
  • Thromosis: due to urinary losses of antithrombin thrombocytosis (steroids), ^clotting factors due to ^haematocrit.
  • Infection: ^risk (including spont peritonitis)
  • Hypercholesterolaemia: correlates inversely with serum albumin.
86
Q

What is Vesicoureteric Reflux?

A

Development anomaly of the vesicoureteric junction: retrograde flow of urine from bladder towards kidney.
A/w: pyelonephritis, scarring, bladder pathology (neuropathic bladder/ urethral obstruction)

87
Q

How is Vesicoureteric Reflux investigated?

A

Imaging: cystogram- contrast outlines ureters + renal collecting ducts.
DMSA scan: scarring.

88
Q

Management of Vesicoureteric Reflux?

A
  • Longterm abx prophylaxis (trimeth/nitro), w/surveillance of renal growth.
  • Surgery if severe reflux
  • Tends to resolve with age!
89
Q

Presentation of Posterior Urethral Valves? (only in boys!)

A
  • Cystogram: dilated posterior urethra, normal anterior urethra. Keyhole appearance of bladder.
  • UTI, abnormal voiding.
90
Q

What should be excluded in bilateral hydronephrosis in a male infant?

A

Posterior urethral valves

91
Q

What is the most common seizure-mimic?

A

Syncope leading to an anoxic (non-epileptic) tonic-clonic seizure.

92
Q

What are some examples of seizure-mimics?

A
  • Breath holding spells (sort of like tantrum, holds breath + goes blue, rapid recovery)
  • Reflex anoxic seizure (minor pain/cold/fright, stops breathing + goes pale, rapid recovery. Due to cardiac asystole from vagal inhibition)
  • Benign paroxysmal vertigo
  • Tics
  • Behaviour disorders
93
Q

(movement disorders)

Presentation of Corticospinal (pyramidal) tract disorders?

A
  • Weakness of distal joints.
  • Brisk hyper-reflexia + extensor plantars.
  • Fine finger movement lost.
94
Q

(movement disorders)

Presentation of Basal Ganglia Disorders?

A

Either:
-Difficulty initiating movements with dystonia, dyskinesia, chorea.
Or;
-Writhing movements (athetosis)

95
Q

(movement disorders)

Presentation of Cerebellar disorders?

A
  • Difficulty holding posture (especially when eyes closed)
  • Past pointing (dysmetria)
  • Dysdiadochokinesis
  • Scanning dysarthria
  • Wide based gait
  • Nystagmus
96
Q

(peripheral motor disorders)

Disorders of the anterior horn cell?

A
  • Spinal muscular atrophy
  • Poliomyelitis

Signs of denervation (weakness, loss of reflexes, fasciculation + wasting)

97
Q

(peripheral motor disorders)

Disorders of the peripheral nerve?

A
  • Bell palsy
  • Acute post-infection (Guillain-Barre)

Often distal nerves affected.
Motor or Sensory neuropathy, + loss of reflexes in either.

98
Q

(peripheral motor disorders)

Disorders of neuromuscular transmission?

A

-Myasthenia gravis.

As end-plate acetylcholine stores become depleted, there is diurnal worsening through the day leading to fatiguability.

99
Q

(peripheral motor disorders)

Muscle disorders? (myopathy)

A
  • Muscle dystrophies (Duchenne/ Becker)
  • Inflammatory myopathies (polymyositis/dermatomyositis)
  • Metabolic myopathies
  • Congenital myopathies

Weakness (often proximal), wasting + gait disturbance.

100
Q

What is markedly elevated in Duchenne/Becker muscular dystrophy?

A

Serum creatinine phosphokinase.

Year 4 PAEDS (5 decks)

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