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Phase 3A > Paeds 3 (Renal, Derm, ID and Psych) > Flashcards

Paeds 3 (Renal, Derm, ID and Psych) Flashcards

1
Q

What are the signs symptoms of UTI in children?x9

A

fever
lethargy
Irritability
Vomiting
Poor feeding
Urinary frequency
dysuria
abdo pain (suprapubic mainly)
incontinence

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2
Q

What signs in addition to UTI signs indicate acute pyelonephritis?

A

temperature above 38oC
Loin pain or tenderness

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3
Q

What is the management for UTI?

A

All children under 3 months with a fever should start IV antibiotics immediately (e.g. ceftriaxone) + have a full septic screen, consider LP

Oral antibiotics can be considered in children >3 months if they are otherwise well:
trimethoprim, nitrofurantoin, cefalexin, amoxicillin

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4
Q

What are the lifestyle modifications/preventative measures against UTI? x4

A

High fluid intake
Regular voiding
Prevent or treat constipation
Good perineal hygiene

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5
Q

What are the investigations for UTI?

A

MSU (difficult in young children)
clean catch - recommended method
urine collection pads
catheter samples or suprapubic aspiration

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6
Q

What are the important factors on MSU and what do they indicate?

A

Nitrites - suggestive of bacteria in the urine as they break down nitrates to nitrites

Leukocytes - significant rise can indicate infection or other cause of inflammation

Nitrites are a better indication of infection than leukocuytes
If both are present or nitrites are present the patient should be treated as a UTI but not if only leukocytes are present

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7
Q

Which bacteria most commonly cause UTIs?

A

E. coli
Proteus is more common in boys
Pseudomonas may indicate structural abnormality

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8
Q

What are some signs which indicate an atypical UTI?

A
  • seriously ill or septicaemia
  • poor urine flow
  • abdominal or bladder mass
  • raised creatinine
  • failure to respond to suitable antibiotics within 48
    hours
  • infection with atypical (non-E. coli) organisms.
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9
Q

What is enuresis?

A

involuntary urination

diurnal enuresis = inability to control bladder function during the day

nocturnal enuresis = bedwetting at night

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10
Q

What are the normal ages at which children have control of day and nighttime urination?

A

daytime urination by 2 yrs
nighttime urination by 3-4 yrs

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11
Q

What is the difference between primary and secondary nocturnal enuresis?

A

primary means that the child has never managed to be consistently dry at night

secondary is when a child begins wetting the bed following having been dry for at least 6 months

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12
Q

What are the potential causes of primary nocturnal enuresis? x6

A

MC: developmental delay

overactive bladder
fluid intake before bedtime (particularly diuretics like fizzy drinks, juice and caffeine)
Failure to wake + underdeveloped bladder signals
Psychological distress
Secondary causes e.g. constipation, UTI, learning disability or cerebral palsy

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13
Q

What are the causes of secondary nocturnal enuresis x5

A

Urinary tract infection
Constipation
T1 Diabetes
New psychosocial problems
Maltreatment

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14
Q

What are some risk factors for nocturnal enuresis? x6

A

Male
Affected 1st degree relative
Learning disability
Emotional stress
Developmental delay
Abuse or neglect

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15
Q

What are the management steps for nocturnal enuresis?

A

Initial priority is to identify underlying cause - 2 week diary of toileting, fluid intake and bedwetting episodes can be helpful to establish any patterns

Reassurance is also a key part of management as most cases will resolve without medical intervention

Lifestyle changes - reduced fluid intake in evenings, pass urine before bed

Encouragement and positive reinforcement - avoid blame or shame

Treat any underlying causes or exacerbating factors e.g. constipation

Enuresis alarms (device which makes a noise at first sign of bed wetting, waking the child and stopping them from urinating)

Pharmacological treatment (desmopressin and oxybutinin)

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16
Q

What is the pharmacological treatment for nocturnal enuresis?

A

Desmopressin (a synthetic form of ADH acts by reducing the volume of urine produced by the kidneys)

Oxybutinin is an anticholinergic medication which reduces the contractility of the bladder and can be used when there is an overactive bladder causing urge incontinence

Imapramine is a TCA and has been shown to help relax the bladder and lighten sleep

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17
Q

What is the main test used to assess renal function in children?

A

plasma creatinine concentration

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18
Q

Which radiological investigations are used to assess the kidneys and urinary tract in children? x5

A

USS (anatomical assessment but not function - useful for UT dilatation, stones and nephrocalcinosis)

DMSA scan - detects dunctional defects e.g. scar tissue

MCUG - visualises bladder and urethral anatomy, detects VUR and urethral obstruction

MAG3 renogram - measures drainage, used to identify VUR in older children

Abdo x-ray - identifies spinal abnormalities and may identify renal stones

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19
Q

What are some congenital renal abnormalities seen in children? x8

A

Renal agenesis (absence of both kidneys which is fatal)

Multicystic dysplastic kidney (results from the failure of union of the ureteric bud)

Autosomal recessive/dominant polycystic kidney disease (cause large cystic kidneys which cause problems in adulthood)

Pelvic/horseshoe kidneys (lower poles of kidneys fuse at the midline)

Premature division of the ureteric bud

Duplex kidney

Bladder exstrophy

Prune-belly syndrome (absent musculature sydrome)

Posterior urethral valves (tissue at the proximal end of the urethra which causes obstruction of urine output)

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20
Q

What is true phimosis?

A

when the foreskin is pathologically non-retractile

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21
Q

What is the commonest condition which gives rise to a true phimosis?

A

balanitis xerotica obliterans (BXO) - causes progressive scarring of the foreskin which can extend into the glans, meatus and ultimately the urethra

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22
Q

What is paraphimosis?

A

a retracted foreskin which cannot be reduced and can result in compromise of the blood supply to the glans
- emergency treatment is needed to reduce the foreskin

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23
Q

What is the definition of and classic triad of features seen in shaken baby syndrome?

A

Intentional shaking of a child (0-5 years old)

Classic triad:
retinal haemorrhages
subdural haematoma
encephalopathy

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24
Q

What is a cephalohaematoma?

A

a bleed occurring between the periosteal membrane and cranial bone which typically develops several hours after birth and doesn’t cross suture lines. It can take months to resolve.

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25
Q

What is included in the 6-1 vaccine and at what ages are the 3 doses given?

A

Diptheria, pertussis, polio, tetanus, Haemophilus influenza b and hepatitis B

Given at 8, 12 and 16 weeks

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26
Q

What is tested for in neonatal blood spot screening? And when is the test performed?

A

Congenital hypothyroidism
Cystic Fibrosis
Sickle cell disease
Phenylketonuria
Medium chain acyl-CoA dehydrogenase deficiency
Maple syrup urine disease
Isovaleric acidaemia
Glutaric aciduria type 1
Homocystinuria

Performed at 5-9 days of life

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27
Q

What risk factors would be indications for adrenaline auto-injector use to treat generalised allergic reactions?

A

Asthma requiring inhaled steroids
Poor access to medical treatment
Adolescents at higher risk
Nut or insect sting allergies are higher risk
Significant co-morbidities e.g. cardiovascular disease

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28
Q

What are salmon patches? character and location, cause, and prognosis?

A

also known as stork bites or angel kisses

small pink or red patches found between a baby’s eyes or on their eyelids, upper lip and back of the neck

caused by a concentration of immature blood vessels and may be more visible when the baby is crying

normally fade and disappear completely

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29
Q

What are mongolian blue spots/congenital dermal melanocytosis?
character and location, cause, and prognosis?

A

blue, grey or purple coloured areas

most commonly found on the baby’s lower back and buttocks

caused by a concentration of pigmented cells

usually disappear in the 1st 4 years of life

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30
Q

What are strawberry haemangiomas?
character and location, cause, and prognosis?

A

bright or dark red, raised or swollen, bumpy area which looks like a strawberry

mostly occur on the head and develop within the 1st 2 months of life

formed by a concentration of tiny, immature blood vessels

often grow in size for a few months and then slowly start to fade, almost all disappear by age 9

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31
Q

What are port-wine stains?
character and location, cause, and prognosis?

A

flat, pink, red or purple colour birthmarks which vary in size

usually found on the head or neck

caused by a concentration of tiny, dilated capillaries

do not disappear over time and may become darker and thicker as a child gets older, can be linked to more serious problems

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32
Q

What are cafe au lait spots?
character and location, cause, and prognosis?

A

flat, hyperpigmented birthmarks found anywhere on the body

caused by a collection of pigment-producing melanocytes in the epidermis of the skin

Multiple of these birth can be a sign of neurofibromatosis type 1

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33
Q

What is the definition of AKI?

A

A sudden, potentially reversible inability of the kidney to maintain normal body chemistry and fluid balance.

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34
Q

What is the hallmark sign of AKI in children?

A

recent increase in creatinine greater than 1.5x previous result

or a value greater than 1.5x upper limit of the reference interval for age

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35
Q

What are some prerenal causes of AKI?

A

MC cause in children - result of reduced blood flow to kidney
–> drop in GFR

SHOCK + HYPOVOLAEMIA (fluid loss) resulting from:
gastroenteritis (D+V –> volume loss)
burns
sepsis
haemorrhage
nephrotic syndrome

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36
Q

What are some renal causes of AKI?

A

VASCULAR
haemolytic uraemic syndrome (MC)
vasculitis
embolus
renal vein thrombosis

TUBULAR
acute tubular necrosis
ischaemic
toxic - drugs
obstructive

GLOMERULAR
glomerulonephritis

INTERSTITIAL
interstitial nephritis
pyelonephritis

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37
Q

Which drugs are nephrotoxic and known to cause intrarenal disease?

A

NSAIDs (inhibits COX which causes excess vasoconstriction of afferent arteriole)

Aminoglycosides (e.g. gentamycin)

ACE-I/ARBs (results in dilated efferent arterioles decreasing GFR)

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38
Q

What are some post renal causes of AKI?

A

OBSTRUCTION
congenital e.g. posterior urethral valves
acquired e.g. blocked urinary catheter

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39
Q

What scan should be performed within 24hrs in children with moderate/severe AKI?

A

urinary tract USS

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40
Q

What are the principles of management of AKI in children?

A

3Ms

Monitor - regular creatinine bloods, monitoring of hydration and fluid balance using urine output, weight urinalysis and PEWS

Maintain - keeping circulatory volume and perfusion pressure stable

Minimise - review, adjust and monitor meds that may affect renal function adversely e.g. NSAIDs, ACEIs, ARB, aminoglycosides and calcineurin inhibitors, avoid contrast

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41
Q

What are the most common causes of chronic kidney disease in children? x8

A

MC: renal dysplasia +/- reflux
obstructive uropathy
glomerular disease
congenital nephrotic syndrome
tubulointerstitial diseases
renovascular disease
polyscystic kidney disease
metabolic causes

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42
Q

What are the key clinical manifestations of stage 4/5 CKD in children?

A

anorexia and lethargy
polydypsia and polyuria
faltering growth/ growth failure
Bony deformities from renal osteodystrophy (renal rickets)
Hypertension
Acute-on-chronic renal failure (precipitated by infection or dehydration)
Incidental finding of proteinuria
Unexplained normochromic, normocytic anaemia

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43
Q

What are the management priorities for CKD in children?

A

Aims are to prevent symptoms and metabolic abnormalities, to allow normal growth and development and preserve residual renal function

Diet - anorexia and vomiting are common symptoms so caloric supplements and nasogastric or gastrostomy feeding are often needed to optimise growth

Control of salt and water balance and acidosis - salt supplements and free access to water, bicarbonate supplements to prevent acidosis

Anaemia - reduced production of erythropoeitin and circulation of metabolites which are toxi to the bone marrow result in anaemia

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44
Q

What are the stages of CKD and eGFR values?

A

1 >90 Normal or increased GFR with other evidence of renal damage e.g. structural abnormality or persistent haematuria/proteinuria
2 60–89 Slight decrease in GFR but mostly asymptomatic
3 A - 45–59, 3 B - 30–44 = Moderate decreased GFR with or without evidence of other renal damage
4 15–29 Severely decreased GFR with or without evidence of renal damage
5 <15 Established renal failure - renal replacement therapy required

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45
Q

Which metabolic abnormalities can result from AKI? x3 and what are the treatments?

A

metabolic acidosis - sodium bicarb

hyperphosphataemia - calcium carbonate + dietary restriction

hyperkalaemia - calcium gluconate (if ECG changes), salbutamol, calcium exchange resin, glucose + insulin, dietary restriction, dialysis

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46
Q

What is the pathophysiology of nephrotic syndrome?

A

hyperpermeability of the glomerular basement membrane to protein resulting in protein leakage from the blood into the urine

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47
Q

What are 3 other features seen in nephrotic syndrome in addition to the classic triad?

A

classic triad = proteinuria, hypoalbuminaemia, oedema

3 other features:
Deranged lipid profile (high levels of cholesterol, triglycerides and low density lipoproteins)
Hypertension
Hyper-coagulability

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48
Q

What is the most common cause of nephrotic syndrome seen in children <10?

A

minimal change disease (90% of cases)

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49
Q

what are some secondary causes of nephrotic syndrome?

A

Focal segmental glomerulosclerosis
Membranoproliferative glomerulonephritis
Henloch schonlein purpura
Diabetes
Infection e.g. HIV, hepatitis and malaria

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50
Q

what are some symptoms seen in children with nephrotic syndrome?

A

Breathlessness (due to pleural effusions and abdo distension)

Infections like peritonitis, septic arthritis, or sepsis (due to loss of protective immunoglobulins in the urine)

Fatigue
Loss of appetite
Pallor
Frothy urine

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51
Q

What is the management for minimal change disease?

A

corticosteroids +/- cyclophosphamide or cyclosporine (in steroid resistant children)

low salt diet
diuretics to treat oedema
albumin infusion for severe hypoalbuminaemia

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52
Q

What is post-strep glomerulonephritis?

A

where immune complexes made up of streptococcal antigens, antibodies and complement proteins get lodged in the glomeruli and cause inflammation and AKI

occurs 1-3 weeks after a B-haemolytic strep infection e.g. tonsilitis

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53
Q

What occurs in IgA nephropathy

A

IgA deposits in the nephrons of the kidneys causing inflammation –> reduced eGFR, haematuria and proteinuria
related to HSP which is an IgA vasculitis

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54
Q

How are nephrotic and nephritic syndrome distinguished?

A

proteinuria in nephritic syndrome is usually <3.5g per day (within the sub-nephrotic range)

nephrotic syndrome does not usually present with haematuria

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55
Q

What are the clinical features of henloch-schonlein purpura?

A

characterisitc skin rash on extensor surfaces
arthralgia
periarticular oedema
abdo pain
glomerulonephritis

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56
Q

What is Alport syndrome?

A

an X-linked recessive disorder which progresses to end-stage chronic kidney disease by early adult life in males and is associated with nerve deafness and ocular defects

caused by a defect in type IV collagen resulting in multi-system effects

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57
Q

What is vesicoureteric reflux?

A

abnormal backflow of urine from the bladder into the ureter and kidney

ureters are displaced laterally which means that the intramural course of the ureter is shortened and the vesicoureteric junction can’t function properly

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58
Q

What is the gold standard investigation for VUR?

A

Micturating cystourethrogram (MCUG)

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59
Q

What are the stages of VUR

A

1 - reflux into ureter only, no dilatation
2 - reflux into the renal pelvis on micturition
3 - mild/moderate dilatation of the ureter, renal pelvis and calyces
4 - dilatation of the renal pelvis and calyces with moderate ureteral tortuosity
5 - gross dilatation of the ureter, pelvis and calyces with ureteral tortuosity

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60
Q

What is the management for VUR?

A

avoid constipation
avoid excessive bladder filling
prophylactic antibiotics
surgical input from paediatric urology - anti-VUR surgery

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61
Q

What is hypospadias?

A

A congenital condition where the opening of the urethra is on the underside of the penis.

Thought to arise from failure of development of ventral tissues of the penis so is technically a ventral hypoplasia of the penis.

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62
Q

What are 3 key features of hypospadias?

A

Ventral urethral meatus, in 80% on the distal shaft or glans penis

Ventral curvature of the shaft of the penis

Hooded appearance of the foreskin - characteristic in appearance but no functional significance

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63
Q

What is the treatment for hypospadias?

A

referral to paeds specialist for management

mild cases may not require any treatment

Surgery may be performed on functional or cosmetic grounds so that the person can pass urine in a straight line whilst standing and have a straight erection.

Surgery is usually performed in the 1st 2-3 years of life if needed

*Infants with hypospadias must not be circumcised to preserve tissue for reconstruction

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64
Q

What is haemolytic uraemic syndrome?

A

A triad of acute renal failure, microangiopathic haemolytic anaemia and thrombocytopenia.

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65
Q

What is the difference between typical and atypical HUS?

A

Typical HUS - good prognosis, diarrhoeal prodrome, long-term follow up required

Atypical HUS - no diarrhoeal prodrome, may be familial, frequent relapses, can be fatal

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66
Q

What causes HUS?

A

typically secondary to GI infection with verocytotoxin-producing E. coli acquired through contact with farm animals or eating undercooked beef, or, less frequently , shigella.

The Shiga toxin from these organisms enters the GI mucosa and then localises to the endothelial cells of the kidney where it causes intravascular thrombogenesis.

The coagulation cascade is activated and CLOTTING IS NORMAL (different to DIC).

Platelets are consumed in this process and microangiopathic haemolytic anaemia results from damage to red blood cells as they circulate through the microcirculation, which is occluded.

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67
Q

What are the symptoms of HUS? x10

A

Fever
Abdo pain
Lethargy
Pallor
Reduced urine output
Haematuria
Hypertension
Bruising
Jaundice (due to haemolysis)
Confusion

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68
Q

What are the investigations for HUS?

A

bloods
stool culture
clinical diagnosis

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69
Q

What is the treatment for HUS?

A

Medical emergency requiring hospital admission and supportive management :

IV fluids (hypovolaemia)
Anti-hypertensives
Blood transfusions (severe anaemia)
Haemodialysis (severe renal failure)

New treatment - monoclonal anti-terminal complement antibody eculizumab improves prognosis of atypical HUS.

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70
Q

How is candida different to nappy rash?

A

the rash extends into the skin folds
large red macules
well demarcated scaly border
circular pattern to the rash spreading outwards
satellite lesions (small, similar patches of rash near the main rash)

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71
Q

What is eczema?

A

chronic atopic condition caused by defects in the normal continuity of the skin barrier, leading to inflammation in the skin.

Severity varies widely and patients experiences flares when eczema is more problematic.

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72
Q

What are some causes of eczema flare ups? x8

A
  • Bacterial infection, e.g. Staphylococcus, Streptococcus spp.
  • Viral infection, e.g. herpes simplex virus
  • Ingestion of an allergen, e.g. egg
  • Contact with an irritant or allergen
  • Environment: heat, humidity
  • Change or reduction in medication
  • Psychological stress
  • Unexplained
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73
Q

What are the key features of atopic eczema?

A

Significant variations in severity/presentations.
Dry, red, itchy and sore patches of skin over the flexor surfaces and on the face and neck.

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74
Q

What is the goal of eczema management?

A

Key is to create an artificial barrier over the skin to compensate for the defective skin barrier which is done using emollients which are as thick and greasy as tolerated.

Particularly important to use after washing and before bed.

avoid triggers such as sudden changes in temperature, certain dietary products, washing powders and cleaning products.

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75
Q

What is used to treat flare-ups?

A

thicker emollients, topical steroids, “wet wraps” (covering affected areas in a thick emollient and applying a wrap to keep moisture locked in overnight) and treating any complications such as bacterial or viral infections

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76
Q

What are some examples of creams (thin/thick) used in eczema treatment?

A

thin:
E45
diprobase
epaderm

thick:
50:50 ointment (liquid paraffin 50%)
hydromol ointment
diprobase ointment

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77
Q

What steroids are used to treat eczema flare-ups? (mild to v potent)

A

Mild: Hydrocortisone 0.5%, 1% and 2.5%
Moderate: Eumovate (clobetasone butyrate 0.05%)
Potent: Betnovate (betamethasone 0.1%)
Very potent: Dermovate (clobetasol propionate 0.05%)

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78
Q

What is the most common organism causing skin infections in eczema and which antibiotic is used to treat it?

A

staph aureus

flucloxacillin

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79
Q

What is eczema herpeticum? which organisms cause it?

A

A viral skin infection caused by herpes simplex virus or varicella zoster virus

Previously known as Kaposi varicelliform eruption

Usually occurs in a patient with a pre-existing skin condition e.g. atopic eczema or dermatitis.

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80
Q

What is the clinical presentation of eczema herpeticum?

A

widespread, painful, vesicular rash with systemic symptoms e.g. fever, lethargy, irritability and reduced oral intake

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81
Q

What is the management for eczema herpeticum?

A

aciclovir (mild cases oral, more severe cases IV)

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82
Q

What are Stevens-Johnson syndrome and toxic epidermal necrolysis? what’s the difference?

A

a type IV hypersensitivity reaction leads to disproportional immune response causes epidermal necrosis, resulting in blistering and shedding of the top layer of skin

SJS and TEN are a spectrum of the same pathology - Generally, SJS affects less that 10% of body surface area whereas TEN affects more than 10% of body surface area.

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83
Q

What are some causes of SJS/TEN?

A

Medications:
Anti-epileptics
Antibiotics
Allopurinol
NSAIDs

Infections:
Herpes simplex
Mycoplasma pneumonia
Cytomegalovirus
HIV

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84
Q

What are the key symptoms of SJS/TEN?

A

Non-specific symptoms - fever, cough, sore throat, sore mouth, sore eyes and itchy skin

Purple/red rash develops and starts to blister

Few days later the skin starts to break away and shed leaving raw tissue underneath
pain , erythema, blistering and shedding of lips and mucous membranes

Eyes become inflamed and ulcerated

Can also affect the urinary tract, lungs and internal organs

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85
Q

What is the treatment for SJS/TEN?

A

Medical emergencies and patients should be admitted to a dermatology or burns unit for treatment.

Good supportive care is essential, including nutritional care, antiseptics, analgesia and ophthalmology input

Steroids, immunoglobulins and immunosuppressant medications

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86
Q

What are some potential complications of SJS/TEN?

A

Secondary infection
Permanent skin damage
Visual complications

87
Q

What is allergic rhinitis?

A

Caused by an IgE-mediated type 1 hypersensitivity reaction

Hypersensitivity of the nasal mucosa to environmental allergens
Can be seasonal e.g. hay fever, perennial e.g. house dust mite allergy, animal fur/saliva/skin allergies, occupational e.g. school or work environmental allergens

88
Q

WHat are the key symptoms of allergic rhinitis?

A

Runny, blocked and itchy nose
Sneezing
Itchy, red and swollen eyes

89
Q

What is the management for allergic rhinitis?
give some examples of sedating and non-sedating antihistamines

A

Avoid the trigger

Oral antihistamines prior to exposure to reduce allergic symptoms:
Non-sedating - cetirizine, loratadine, fexofenadine
Sedating antihistamines - chlorphenamine, promethazine

Nasal corticosteroid sprays e.g. fluticasone and mometasone

Nasal antihistamines

90
Q

what is urticaria? what causes it and what is it associated with?

A

Urticaria is hives i.e. small itchy lumps that appear on the skin.

They may be associated with angioedema (swelling of the deeper layers of the skin, caused by a build-up of fluid.) and flushing of the skin

Urticaria are caused by the release of histamine and other pro-inflammatory chemicals by mast cells in the skin.

Most common form is spontaneous urticaria which can be acute (<6 weeks) or chronic (>6 weeks)

91
Q

What are some causes of urticaria?

A

Allergens in food or medicine can sometimes cause acute urticaria as well as bee or wasp stings.

Cow’s milk allergy is the most common cause in babies

Often idiopathic

chronic spontaneous urticaria may also be autoimmune or inducible (when they are induced by a specific stimulus and are not spontaneous)

92
Q

What is the managment for urticaria/angioedema?

A

aim of treatment is to suppress symptoms rather than cure it

In around half of people affected by chronic spontaneous urticaria the rash lasts for 6-12 months

Antihistamine can be used to reduce itch and the rash but normally cannot resolve urticaria completely

Oral steroids for severe flares

Immunosuppressants for severely affected people

Adrenaline injection if breathing problems caused by angioedema

93
Q

What is anaphylaxis? what is happening in the body

A

A life-threatening medical emergency caused by severe type 1 hypersensitivity reaction

IgE stimulates mast cells to rapidly release histamine and other pro-inflammatory chemicals (mast cell degranulation)

Causes a rapid onset of symptoms, with airway, breathing and/or circulation compromise.

94
Q

What is a key differentiating feature of anaphylaxis which differentiates it from non-anaphylactic reactions?

A

compromise of the airway, breathing or circulation.

95
Q

What are the key symptoms of anaphylaxis? x6

A

SOB
Wheeze
Stridor (caused by swelling of the larynx)
Tachycardia
Lightheadedness
Collapse

alongside allergic signs like urticaria, ithcing, angioedema, abdo pain

96
Q

What is the management for anaphylaxis?

A

A-E assessment - management by senior paediatrician needed
Intramuscular adrenaline, repeated after 5 mins if required

Antihistamines, e.g. chlorphenamine or cetirizine

Steroids usually IV hydrocortisone

Risk of biphasic reaction so children require post-reaction monitoring

Anaphylaxis can be confirmed by measuring the serum mast cell tryptase within 6 hours of the event

Family and patient education to prevent future attacks

97
Q

What is nappy rash? what age children is it most commonly seen in ?

A

Contact dermatitis in the nappy area
Most common between 9-12 months

98
Q

What causes nappy rash?

A

Normally caused by friction between the skin and nappy and contact with the urine and faeces

Breakdown of skin and the warm moist environment can lead to candida (fungus) pr bacterial infection (staph/strep)

99
Q

What are the risk factors for nappy rash? x5

A

Delayed changing of nappies
Irritant soap products and vigorous cleaning
Diarrhoea
Oral antibiotics predispose to candida
Preterm infants

100
Q

What are the key features of nappy rash?

A

Sore, red, inflamed skin in the nappy areas
No rash on the creases of the groin
Distressed infant
Severe and long standing rash can lead to erosion and ulceration

101
Q

What is the management for nappy rash?

A

Switch to highly absorbent nappies
Change the nappy and clean the skin asap after wetting or soiling
Use water or gentle alcohol free products
Ensure the nappy area is dry before replacing the nappy
Maximise rime not wearing a nappy
Infection requires antifungal/antibiotic cream

102
Q

What is infantile seborrhoeic dermatitis? how does it present?

A

Eruption of unknown cause which presents in the first 3 months of life

Starts on the scalp as an erythematous scaly eruption

The scales form a thick yellow adherent layer, commonly called cradle cap

The scaly rash may spread to the face, behind the ears and then extend to the flexures and nappy area.

Associated with an increased risk of developing atopic eczema

103
Q

What is the management for infantile seborrhoeic dermatitis?

A

Mild cases will resolve with emollients

The scales on the scalp can be cleared with an ointment containing low-concentration sulphur and salicylic acid

Widespread body eruption will clear with a mild topical corticosteroid which can be mixed with an antibacterial and antifungal agent if required.

104
Q

What is an exanthem? what were the 6 viral exanthemas?

A

an eruptive widespread rash

First disease: Measles
Second disease: Scarlet Fever
Third disease: Rubella (AKA German Measles)
Fourth disease: Dukes’ Disease
Fifth disease: Parvovirus B19
Sixth disease: Roseola Infantum

105
Q

What is measles? spread? presentation? symptoms? prognosis?

A

a highly contagious viral illness caused by the measles virus

spread by respiratory droplets

symptoms start 10-12 days post-exposure

fever, coryzal symptoms + conjunctivitis

self-resolving after 7-10 days of symptoms

NOTIFIABLE

106
Q

What is the character of the measles rash? what, where, when in viral illness?

A

koplik spots (greyish white spots on the tongue (buccal mucosa))

rash starts on the face, classically behind the ears, 3-5 days after the fever and then spread to rest of body

erythematous, macular rash with flat lesions

107
Q

What are the potential complications of measles? x8

A

Pneumonia
Diarrhoea
Dehydration
Encephalitis
Meningitis
Hearing loss - otitis media
Vision loss
Death

108
Q

What is scarlet fever? spread? presentation? symptoms? prognosis?

A

group A streptococcus infection, usually tonsillitis

respiratory droplet spread

fever, lethargy, flushed face, sore throat, strawberry tongue. cervical lymphadenopathy

resolves with antibiotics

NOTIFIABLE

109
Q

what causes scarlet fever?

A

an exotoxin produced by the streptococcus pyogenes (group A strep) bacteria

110
Q

Describe the rash seen in scarlet fever

A

red-pink, blotchy, macular rash with rough ‘sandpaper’ skin which starts on the trunk and spreads outwards

patients often have red, flushed cheeks

111
Q

What is the treatment for scarlet fever?

A

phenoxymethylpenicillin (penicillin V) for 10 days

112
Q

What other 2 conditions are associated with group A strep infections alongside scarlet fever?

A

Post-streptococcal glomerulonephritis
Acute rheumatic fever

113
Q

What is rubella?

A

highly contagious viral illness caused by rubella virus

spread by respiratory droplets

symptoms start 2 weeks after exposure

mild fever, joint pain and a sore throat with lymphadenopathy

self-limiting requiring supportive treatment

NOTIFIABLE

114
Q

describe the rash seen in rubella

A

erythematous macular rash which starts on the face and spreads to the rest of the body

usually lasts 3 days

milder than measles rash

115
Q

What are the potential complications of rubella? why should infected children avoid pregnant women?

A

thrombocytopenia
encephalitis

rubella is dangerous in pregnancy and can lead to congenital rubella syndrome which is a triad of deafness, blindness and congenital heart disease

116
Q

What is slapped cheek syndrome (Parvovirus b19)?

A

infection caused by parvovirus B19

spread by droplets

mild fever, coryza and non-specific viral symptoms like muscles aches and lethargy

self-limiting and rash and symptoms usually fade over 1-2 weeks

117
Q

Describe the rash in slapped cheek syndrome

A

diffuse bright red rash on both cheeks as though they’ve been slapped - presents after 2-5 days of fever

followed by reticular (net-like) mildly erythematous rash affecting the trunk and limbs which can be raised and itchy

118
Q

Which patients are at risk of complications with slapped cheek syndrome? what tests do they require?

A

immunocompromised patients, pregnant women
patients with haematological conditions (such as sickle cell anaemia, thalassaemia, hereditary spherocytosis and haemolytic anaemia.)

these patients should have serology testing for parvovirus to confirm the diagnosis and check for aplastic anaemia

119
Q

What are the potential complications of slapped cheek syndrome?

A

Aplastic anaemia
Encephalitis or meningitis
Pregnancy complications including fetal death
Rarely hepatitis, myocarditis or nephritis

120
Q

What is roseola infantum?

A

caused by human herpesvirus 6 (HHV-6) and less frequently by human herpesvirus 7 (HHV-7

presents 1 – 2 weeks after infection with a high fever (up to 40ºC) that comes on suddenly, lasts for 3 – 5 days and then disappears suddenly.

coryzal symptoms, sore throat and swollen lymph nodes

full recovery within a week

121
Q

Describe the rash seen in roseola infantum

A

mild erythematous macular rash across the arms, legs, trunk and face and is not itchy.

122
Q

What is the main complication resulting from roseola infantum?

A

febrile convulsions due to high temperature.

123
Q

What is chickenpox?

A

common and highly contagious viral illness caused by the varicella zoster virus

124
Q

What is the clinical presentation of chicken pox?

A

widespread, erythematous, raised, vesicular (fluid filled), blistering lesions

rash usually starts on the trunk or face and spreads outwards affecting the whole body over 2 – 5 days

associated with fever, itching and general fatigue/malaise

125
Q

How is chickenpox spread?

A

direct contact with the lesions or through infected droplets from a cough or sneeze

patients stop being contagious after al the lesions have crusted over

126
Q

What are the potential complications of chickenpox? x5

A

Bacterial superinfection
Dehydration
Conjunctival lesions
Pneumonia
Encephalitis (presenting as ataxia)

127
Q

What is congenital varicella syndrome?

A

when a women contracts chickenpox in pregnancy, before 28 weeks gestation resulting in developmental problems in the fetus

128
Q

what is the management for chicken pox?

A

usually mild and self-limiting not requiring treatment

in immunocompromised patients and neonates aciclovir may be considered

129
Q

What is staphylococcal scalded skin syndrome? what causes it?

A

caused by a type of staphylococcus aureus bacteria that produces epidermolytic toxins.

These toxins are protease enzymes that break down the proteins that hold skin cells together. When a skin infection occurs and these toxins are produced, the skin is damaged and breaks down.

130
Q

What is the presentation of SSSS?

A

generalised patches of erythema on the skin

thin and wrinkled-looking skin

fluid filled blisters called bullae which burst leaving sore, erythematous skin below which appears similar to a burn or scald

nikolsky skin where very gentle rubbing of the skin causes it to peel away

systemic symptoms: fever, irritability, lethargy, dehydration

131
Q

what is the management for staphylococcal scalded skin syndrome?

A

admission and treatment with IV antibiotics e.g. flucloxacillin

analgesia

fluid and electrolyte balance

132
Q

What is impetigo?

A

a localised, highly contagious, staph or strep skin infection

more commonly occurs in infants and young children

133
Q

What is characterisitic of a staphylococcus aureus infection in impetigo?

A

a golden crust

134
Q

What is the difference between bullous and non-bullous impetigo?

A

non-bullous typically occurs arouns the nose or mouth and does not usually cause systemic symptoms

bullous impetigo is always caused by staph aureus and is more commonly seen in neonates and infants <2yrs causing systemic symptoms and general malaise

135
Q

What is the treatment for impetigo? bullous/non-bullous

A

topical fusidic acid for non-bullous

oral flucloxacillin in bullous and more widespread/severe cases of non-bullous

advise about spread prevention - don’t scratch, wash hands, don’t share cutlery/clothes/towels

136
Q

Describe the vesicles seen in bullous impetigo?

A

1-2 cm fluid vesicles which grow in size and then burst forming a golden crust

the lesions can be painful and itchy

137
Q

What are some potential complications of impetigo? x6

A

Cellulitis if the infection gets deeper in the skin
Sepsis
Scarring
Post streptococcal glomerulonephritis
Staphylococcus scalded skin syndrome
Scarlet fever

138
Q

What is whooping cough?

A

an infectious disease caused by the gram-negative bacterium bordatella pertussis

139
Q

When are children immunised against whooping cough?

A

at 8, 12 and 16 weeks and 3-5 years

140
Q

What are the 3 phases of whooping cough infection?

A
  1. Catarrhal phase
    - Symptoms similar to viral URTI e.g. runny nose, fever, cough, sore throat
    - Lasts around 1-2 weeks
  2. Paroxysmal phase
    - Cough increases in severity and characteristic inspiratory whoop can be present
    - Lasts between 2-8 weeks
  3. Convalescent phase
    - cough subsides over weeks to months
141
Q

What is the diagnostic criteria for whooping cough?

A

Acute cough lasting for 14 days or more without another apparent cause and has one or more of the following features:
- Paroxysmal cough
- Inspiratory whoop
- Post-tussive vomiting
- Undiagnosed apnoeic attacks in young infants

142
Q

What is the management for whooping cough?

A

Admit infants under 6 months

Oral macrolide e.g. clarithromycin, azithromycin or erythromycin (indicated if the onset of the couth is within the previous 21 days)

Antibiotic prophylaxis for household contacts

School exclusion 28 hours after commencing antibiotics

NOTIFIABLE disease

143
Q

What is diphtheria and how does it present?

A

usually mild infection caused by the bacterium corynebacterium diphtheriae

symptoms often develop gradually, beginning with a sore throat and fever

in severe cases, a grey or white patch develops in the throat, which can block the airway and create a barking cough similar to what is observed in croup

may involve lymph node swelling and can involve skin, eyes and genitals

rarely seen in UK due to effective vaccinations

144
Q

What is polio? in which countries is it still endemic?

A

Polio is the common name of poliomyelitis, a highly contagious disease caused by a poliovirus which usually affects children <5yrs old.

remains endemic in afghanistan and pakistan

145
Q

What is the presentation of polio?

A

often asymptomatic (75%)
mild symptoms: sore throat and fever
more severe: headache, neck stiffness and paraesthesia

more rarely: paralysis and post-polio syndrome (years after)

146
Q

What is the treatment?

A

there is no special treatment, only supportive which makes the vaccine extremely important

147
Q

What is tuberculosis? what is special about the bacteria?

A

an infectious disease caused by mycobacterium tuberculosis

these bacilli have a waxy coating which means they are acid-fast and require Zeihl-Neelsen stain to be identified

148
Q

What are the potential outcomes once infected with TB? x6

A

immediate clearance of the bacteria (most cases)

primary active TB (active infection after exposure)

latent tuberculosis (presence of the bacteria without being symptomatic or contagious)

secondary tuberculosis (reactivation of latent TB to active infection)

miliary tuberculosis (disseminated and severe disease resulting from inability of the immune system to control the infection)

extrapulmonary tuberculosis (TB affecting organs outside of the lungs)

149
Q

What are the risk factors for TB?

A

Close contact with active tuberculosis (e.g., a household member)

Immigrants from areas with high tuberculosis prevalence

People with relatives or close contacts from countries with a high rate of TB

Immunocompromised (e.g., HIV or immunosuppressant medications)

Malnutrition, homelessness, drug users, smokers and alcoholics

150
Q

What is the BCG vaccine and how does it work?

A

Bacillus Calmette-guerin vaccine is an intradermal injection of live attenuated mycobacterium bovis bacteria which creates an immune response and provides immunity against M. tuberculosis without causing infection

151
Q

What are the common signs and symptoms of TB? x8

A

Cough
Haemoptysis (coughing up blood)
Lethargy
Fever or night sweats
Weight loss
Lymphadenopathy
Erythema nodosum (tender, red nodules on the shins caused by inflammation of the subcutaneous fat)
Spinal pain in spinal tuberculosis (also known as Pott’s disease of the spine)

152
Q

What are the investigations used to diagnose TB?

A

sputum culture with Z-N stain

latent or active TB can be detected by mantoux test or interferon-gamma release assay

153
Q

What are the signs of disseminated/miliary TB on CXR?

A

Patchy Consolidation
Ghon Complex (a focal caseating granuloma)
Granulomatous Lesions
Hilar Lymphadenopathy - (enlargement)
Pleural Effusion

154
Q

What is the treatment for active TB?

A

RIPE - combination antibiotics for 6-12 months

R - Rifampicin for 6 mo
I - Isoniazid for 6 mo
P – Pyrazinamide for first 2 months
E – Ethambutol for first 2 months

155
Q

What are the side effects of the TB antibiotic treatments?

A

Rifampicin - haematuria and hepatotoxic
Isoniazid - peripheral neuropathy and hepatotoxic
Pyrazinamide - hyperuricaemia, arthralgia and hepatotoxic
Ethambutal - optic neuritis e.g. uveitis

156
Q

How is HIV spread?

A

Unprotected anal, vaginal or oral sexual activity

Mother to child at any stage of pregnancy, birth or breastfeeding. This is referred to as vertical transmission.

Mucous membrane, blood or open wound exposure to infected blood or bodily fluids. This could be through sharing needles, needle-stick injuries or blood splashed in an eye.

157
Q

How is the mode of delivery for giving birth determined for mothers with HIV?

A

Normal vaginal delivery is recommended for women with a viral load <50 copies/ml

Caesarean sections are considered in patients with >50 copies/ml and in all women with >400 copies/ml

IV zidovudine should be given during the caesarean if the viral load is unknown or there are >10000 copies/ml

158
Q

Outline the prophylactic treatment for babies at risk of HIV. Can HIV positive mothers breastfeed?

A

Prophylaxis treatment may be given to the baby depending on viral load:

  • low risk babies where mother’s viral load is <50 copies/ml should be given zidovudine for 4 weeks
  • high risk babies with maternal viral load of >50 copies/ml should be given zidovudine, lamivudine and nevirapine for 4 weeks

No - HIV can be transmitted during breastfeeding

159
Q

When should you test for HIV in children with HIV positive parents

A

Babies to HIV positive parents are tested twice for HIV:

HIV viral load test at 3 months. If this is negative, the child has not contracted HIV during birth and will not develop HIV unless they have further exposure.

HIV antibody test at 24 months. This is to assess whether they have contracted HIV since their 3 month viral load, for example through breast feeding. If the 3 month test is negative and they are not breastfed, this should be negative.

Note that the antibody test can be positive in infants who do not have HIV for up to 18 months of age. This is due to maternal antibodies that have crossed the placenta during pregnancy.

160
Q

What is the treatment for paediatric HIV?

A

Antiretroviral therapy (ART) to suppress the HIV infection

Normal childhood vaccines, avoiding or delaying live vaccines if severely immunosuppressed.

Prophylactic co-trimoxazole (Septrin) for children with low CD4 counts, to protect against pneumocystis jirovecii pneumonia (PCP)

Treatment of opportunistic infections

The aim of antiretroviral therapy (ART) is to achieve a normal CD4 count and undetectable viral load

161
Q

What are the common bacterial causes of meningism in neonates (0-3mo)?

A

E. coli
Group B streptococcus
Listeria monocytogenes

162
Q

What are the common causes of bacterial meningitis in infants (1mo-6yrs)?

A

Neisseria meningitidis
Haemophilus influenzae
Streptococcus pneumoniae

163
Q

What are the common causes of bacterial meningitis in older children/young adults (>6yrs)?

A

Neisseria meningitidis
Streptococcus pneumoniae

164
Q

Which viruses can cause meningitis? x3

A

enteroviruses (e.g. coxsackievirus)
herpes zoster virus
varicella zoster virus

165
Q

What are the fungal causes of meningitis?

A

cryptococcus, histoplasma, blastomyces

166
Q

What are some signs of meningitis?

A

Kernig’s sign: extension of the knee when hip is flexed at 90 degrees causes neck pain
Brudzinski sign: severe neck stiffness causes the hips and knees to flex when the neck is flexed
Petechial or purpuric non-blanching rash: associated with meningococcal disease (N. meningitidis)
Pyrexia
Reduced GCS

167
Q

What are some symptoms of meningitis?

A

FEVER
HEADACHE
NECK STIFFNESS – ‘MENINGISM’
Might not be able to touch chin to neck
Purpuric rash – only in BACTERIAL meningitis
Non-blanching purpurent rash = meningococcal septicaemia (meningitis caused by N. Menigitidis)
Photophobia and/or phonophobia
Papilloedema – swelling of optic disc on fundoscopy
Usually bilateral

168
Q

What are the investigations for meningitis?

A

INVESTIGATIONS AND TREATMENT SHOULD BE DONE IN PARALLEL

Treat first, investigate later – give IM benzylpenicillin
Assess GCS - if <8 then can’t maintain their own airway, 🡪 intubate

Blood cultures – BEFORE ANTIBIOTICS!!

Lumbar puncture - to obtain CSF - Diagnostic
Head CT – to exclude lesions e.g. tumour

Blood – blood cultures and PCR for S. pneumoniae and N. meningitidis.
Nose and throat swabs – are plated out onto blood and chocolate agar.
Stool – stool PCR can be used to detect enterovirus.

Serology – blood (to detect a convalescent rise in antibody).

169
Q

When do NICE recommend a lumbar puncture as part of the investigations for all children under 1 month, 1-3 months and 1 year?

A

NICE recommends a lumbar puncture as part of the investigations for all children:

Under 1 month presenting with fever
1 to 3 months with fever and are unwell
Under 1 year with unexplained fever and other features of serious illness

As v young kids have a BBB that is far easier to penetrate

170
Q

What CSF changes are seen in bacterial meningitis?

A

Increased opening pressure
Cloudy yellow appearance
Increased WCC (neutrophilia)
Increased protein (>1g/L)
Decreased glucose (<50% serum level)

bacteria swimming in the CSF (cloudy) will release proteins (high) and use up the glucose (low). Immune response to bacteria is neutrophils

171
Q

What CSF changes would be seen on LP in viral meningitis?

A

Normal opening pressure
Clear, normal colour CSF
Increased WCC (lymphocytosis)
Normal protein levels
Increased glucose (>60% serum level)

Viruses cant be seen (clear) don’t use glucose (normal) but may release a small amount of protein (normal/mild inc). Immune response to viruses are lymphocytes

172
Q

What are the CSF changes seen in fungal meningitis?

A

Increased opening pressure
Cloudy + fibrinous appearance
Increased WCC (lymphocytosis)
Increased protein (>1g/L)
Decreased glucose (<50% serum level)

173
Q

What is the treatment for viral meningitis?

A

usually milder and so supportive treatment

if HSV/VZV infection treat with aciclovir

174
Q

What is the treatment for bacterial meningitis in a hospital, for those <60 and not immunocompromised?

A

IV dexamethasone, ideally administered before or with the first dose of antibiotics once in hospital. Reduces mortality and likelihood of neurological sequelae.

ceftriaxone : 2 g intravenously every 12 hours
OR
cefotaxime : 2 g intravenously every 6 hours

175
Q

What is the treatment for suspected meningitis with non-blanching rash present in the community?

A

urgent/immediate IM Benzylpenicillin
prior to immediate transfer to a hospital

176
Q

What are some things that neonates may present with that should make you think of meningitis?

A

Neonates and babies can present with very non-specific signs and symptoms, such as hypotonia, poor feeding, lethargy, hypothermia and a bulging fontanelle.

Any Fever, unless obvious source - need to rule out meningitis

177
Q

What is the most common cause of Encephalitis, in
a) Children
b) Neonates

A

In children the most common cause is herpes simple type 1 (HSV-1) from cold sores.

Neonates it is herpes simplex type 2 (HSV-2) from genital herpes, contracted during birth

178
Q

What are some syptoms that children get in Encephalitis? x6

A

Altered consciousness
Altered cognition
Unusual behaviour
Acute onset of focal neurological symptoms
Acute onset of focal seizures
Fever

179
Q

Which viruses can cause encephalitis? x6

A

Herpes simplex
varicella zoster
parvoviruses
HIV
mumps
measles

180
Q

What are the investigations for encephalitis?

A

lumbar puncture + CSF analysis (viral PCR testing)
MRI head (GS)
EEG recording
swabs
HIV testing

181
Q

What is the management for encephalitis?

A

Intravenous antiviral medications are used to treat the suspected or confirmed underlying cause:

Aciclovir treats herpes simplex virus (HSV) and varicella zoster virus (VZV)
Ganciclovir treat cytomegalovirus (CMV)

Repeat lumbar puncture is usually performed to ensure successful treatment prior to stopping antivirals

Aciclovir is usually started empirically in suspected encephalitis until results are available. Other viral causes have no effective treatment and management is supportive.

182
Q

What is the treatment for candida?

A

topical antifungal e.g. imidazole

stop using a barrier cream until the candida has settled

183
Q

What is toxic shock syndrome? which bacteria are responsible

A

a severe systemic reaction ot staphylococcal exotoxin

toxin-producing S.aureus and group A strep

184
Q

What can cause toxic shock syndrome?

A

leaving tampons in too long
femal barrier contraceptives
any break in the skin
nasal packing for nose bleeds

185
Q

What is the characteristic presentation of toxic shock syndrome?

A
  • fever over 39° C
  • hypotension
  • diffuse erythematous, macular rash.
186
Q

Which organs can be affected in toxc shock syndrome?

A

mucositis: conjunctivae, oral mucosa, genital mucosa
GI: vomiting/diarrhoea
renal impairment
liver impairment
clotting abnormalities and thrombocytopenia

187
Q

What is the management for toxic shock syndrome?

A

medical emergency
intensive care support is needed to manage the shock and areas of infection should be debrided

abx such as ceftriaxone with clindamycin are used to stop toxin production

188
Q

What are the primitive reflexes?

A

Primitive reflexes are reflex actions from CNS, seen in normal infants, but not neurologically intact adults, in response to particular stimuli.

These reflexes are suppressed by the development of the frontal lobes as a child transitions normally into child development.

eg Moro, Grasp, and Galant

189
Q

What is the grasp reflex?

A

When an object is placed in the infant’s hand and strokes their palm, the fingers will close and they will grasp it with a palmar grasp

190
Q

What is the moro reflex?

A

Said to be the only unlearned fear in newborns, a reflex done by a startling baby

It is likely to occur if the infant’s head suddenly shifts position, the temperature changes abruptly, or they are startled by a sudden noise. The legs and head extend while the arms jerk up and out with the palms up and thumbs flexed, then infant pulls his arms and legs in and starts crying

191
Q

What is the galant reflex?

A

When the skin along the side of an infant’s back is stroked, the infant will swing towards the side that was stroked.

192
Q

Why should primitive reflexes disappear?

A

Primitive reflexes should gradually disappear as postural reflexes develop. This essential for good motor development.

If they persist, There may be a sign of CNS dysfunction

193
Q

What are the 4 domains of child development?

A
  1. Gross motor.
  2. Fine motor and vision.
  3. Speech, language and hearing.
  4. Social interaction and self care skills
194
Q

What are the gross motor milestones?

A

3 mo - good head control, little-no head lag, held sitting

6 mo - sits without support, rounded back, rolls front to back

7-9 mo - straight back sitting, pulls to standing, crawling

12-15 months - cruising to walking unsupported

18 mo - runs, jumps

2 yrs - runs on tiptoes, walks up stairs both feet, throws ball

3 yrs - hops

4 yrs - up and down stairs like adult

195
Q

what are the developmental milestones for fine motor and vision?

A

3 mo - reaches for object, responds to light/sound, makes fist, fixes and follows to 180 degrees

6 mo - palmar grasp, hand transfers

9 mo - inferior pincer grip, points with 1 finger

12 months - good pincer grip, bangs toys together, casting

18 mo - 4 bricks, circular scribble

2 yrs - 8 bricks, vertical line, turns several pages of book

3 yrs - copies circle, bridge or train with bricks, turns single page

4 yrs - copies cross/square, 12 blocks/steps

196
Q

What are the speech and language developmental milestones?

A

3 mo - stills, startles at loud noise

6 mo - turns head to loud sounds, double syllables, babbles

9 mo - responds to own name, understands no

12-15 months - knows 2-6 words, understands simple commands

18 mo- 2yrs - combiines 2 words, points to parts of the body

3 yrs - 3-4 words joined together, what and who questions, colours, counts to 10

4 yrs - why, when, how questions, understands complex instructions

197
Q

What are the developmental milestones for social behaviour and play?

A

2 mo - social smile

6 mo - laughs, objects to mouth, shakes rattle, reaches for food

9 mo - stranger danger, holds food

12 months - waves bye, hand clapping, parallel play, drinks from beaker with lid

18 mo - imitates everyday activities

2 yrs - eats with spoon

3 yrs - starts sharing toys, plays alone, eats with spoon/fork, bowel control

4 yrs - shows sympathy, has a best friend, bladder control

5 yrs - imaginative play, handles knife, dress/undress

198
Q

What are 2 examples of red flags in a child’s gross motor development?

A

not sitting by 12 months

not walking independently by 2 yrs

199
Q

What are 2 examples of red flags in a child’s fine motor development?

A

no pincer grip at 12 mo

not attempting to feed self using a spoon or help with dressing at 2 yrs

200
Q

What are 2 examples of red flags in speech and language development?

A

no babbled phrases at 12 mo

no words or unable to understand simple requests at 18mo -2yrs

201
Q

what is an example of concerning child development in terms of fine motor function?

A

hand preference before 18 mo

202
Q

What are 2 examples of social developmental red flags

A

no smile at 6 months

no interest in playing by 3 yrs

203
Q

What is autistic spectrum disorder?

A

refers to the full range of people affects by a deficit in social interaction, communication and flexible behaviour

204
Q

What are some examples of the deficits in social interaction seen in children with ASD? x6

A

lack of eye contact
delay in smiling
avoids physical contact
unable to read non-verbal cues
difficulty establishing friendships
not displaying a desire to share attention (i.e. not playing with others)

205
Q

What are some examples of communication deficits seen in children with ASD?

A
  • delay, absence or regression in language development
  • lack of appropriate non-verbal communication such as smiling, eye contact, responding to others and sharing interests
  • difficulty with imaginative or imitative behaviour
  • repetitive use of words and phrases
206
Q

What are some examples of behavioural deficits seen in children with ASD?

A
  • greater interest in objects, numbers or patterns than people
  • stereotypical repetitive movements e.g. hand-flapping or rocking.
  • Intensive and deep interests that are persistent and rigid
  • Repetitive behaviour and fixed routines
  • Anxiety and distress with experiences outside their normal routine
  • Extremely restricted food preferences
207
Q

At what age does ASD commonly first present?

A

2-4 years

208
Q

How is global developmental delay defined?

A

a child displaying slow development in all developmental domains

209
Q

Diagnosis of which conditions could be indicated by global developmental delay? x5

A

Down’s syndrome
Fragile X syndrome
Fetal alcohol syndrome
Rett syndrome
Metabolic disorders

210
Q

Which conditions are associated with gross motor delay? x5

A

Cerebral palsy
Ataxia
Myopathy
Spina bifida
Visual impairment

211
Q

Which conditions are associated with fine motor delay? x5

A

Dyspraxia
Cerebral palsy
Muscular dystrophy
Visual impairment
Congenital ataxia (rare)

212
Q

Which conditions are associated with language delay ( x6 but some not rlly conditions)

A

Specific social circumstances, (for example exposure to multiple languages or siblings that do all the talking)
Hearing impairment
Learning disability
Neglect
Autism
Cerebral palsy

213
Q

At what age does global developmental delay usually present?

A

within the first 2 years of life

Phase 3A (10 decks)

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