Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Paediatrics (Y4) > Acute presentations > Flashcards

Acute presentations Flashcards

1
Q

sepsis

A
  • Sepsis is a life-threatening illness caused by the body’s response to an infection.
  • Recognising sepsis is often very difficult in children as symptoms and signs can be similar to self- limiting or less severe conditions.
  • Bacterial infections are by far the commonest cause of sepsis (can be viral or fungal).
  • Sepsis is defined as suspected/proven infection with Systemic Inflammatory Response (SIRS).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

presentation of sepsis

A

SIRS is the presence of at least 2 of the following:

One of which must be temperature or WCC

  • Core temperature > 38.5oC or < 36oC.
  • Tachycardia (in absence of external stimuli). Tachypnoea for age (or ventilation).
  • White cell count elevated or depressed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

screening for sepsis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

managment of sepsis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

anaphylaxis

A
  • Severe, life-threatening allergic reaction that is acute in onset and can cause death.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

differentials for anaphylaxis

A
  • Skin: Acute urticaria.
  • GUT: Food poisoning, gastroenteritis.
  • Respiratory: URTI, irritant rhino-conjunctivitis, choking, viral wheeze. acute asthma exacerbation.
  • CVS: vasovagal syncope, panic attack.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

presentation of anaphylaxis

A
  • Angioedema same pathophysiology as urticaria, however occurs in deeper layer of the skin with no itch receptors therefore not itchy like acute urticaria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

management of suspected anaphylaxis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

classic history for acute urticaria

A
  • Woke this morning with rash:
  • Raised erythematous plaques.
  • Some have pale centre.
  • Rash spreading; plaques coalescing.
  • Rash intensely pruritic.
  • Agitated, irritable and unhappy.
  • No previous allergies; eats all foods.
  • No recent new contact – food, drug.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

acute urticaria background

A
  • Also called hives, wheals or welts.
  • Common condition affecting up to 20% of population.
  • Typically intensely pruritic erythematous plaque.
  • May be associated with angioedema (swelling).
  • Commonly categorized by chronicity:
  • Acute: <6 weeks; triggers allergy, URTI, idiopathic.
  • Chronic: >6 weeks; spontaneous or physical triggers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

presentation of acute urticaria

A

Presentation
- Intensely pruritic rash
- Agitated, irritable, unhappy
- Spreading rash
- Raised erythematous plaques

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

management of acute urticaria

A
  • History and examination to make diagnosis.
  • In new-onset acute urticaria where assessment does NOT suggest underlying cause, NO investigations; may consider FBC and CRP if worried about vasculitis.
  • High-dose non-sedating antihistamines.
  • ± Oral glucocorticosteroids.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

paracetamol overdose protocol overview 1/2

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

history for paracetamol overdose

A

o Dose
o Timing
o Associated ingestions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

paracetamol overdose protocol overview 2/2

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

management of paractermaol overdose

A

charcoal only if very recently ingested

defintive treatment: N-acetylcysteine infusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

differential diagnosis

A

* Pre-septal cellulitis.
* Orbital or Post-septal cellulitis. * Allergicconjunctivitis.
* Bacterial conjunctivitis.
* Trauma.
* Sub-periostal/orbital abscess. * Cavernous sinus thrombosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

history and examiantion for red swollen eye

A
  • Acuity of onset?
  • Recent URTI?
  • Local insect bite, impetigo or conjunctivitis?
  • Trauma?
  • Eye pain, visual acuity, headache?
  • Erythema/swelling of lid/surrounding tissue.
  • Conjunctiva – white or red/swollen.
  • Impaired eye movement (ophthalmoplegia).
  • Painful eye movements.
  • Impaired visual acuity.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

presentation of pre-septal and orbital cellulitis

A

Pre-septal cellulitis

  • Ocular itching is a prominent symptom.
  • Bilateral conjunctival redness and swelling.
  • Symptoms on exposure.
    **Conjunctivitis **
  • Redness and discharge from one eye.
  • Affected eye ‘stuck shut’ in the morning.
  • Colour/consistency depends on cause.
  • Caused by bacteria (Staph. Aureus, H. Strep,
    H. Influenzae) chlamydia, viruses.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

pre-septal vs orbital cellulitis

A

Pre-septal cellulitis: inflammatory disease of the orbit limited to the tissues anterior to the orbital septum.

Orbital cellulitis: inflammatory disease of the superficial and deep structures of the orbit.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

aetiology of pre-septal cellulitis

A
  • 85%+ cases are pre-septal cellulitis.
  • Commonly follows URTI and sinusitis (ethmoid commonest).
  • Respiratory pathogens (Streptococcus, Haemophilus) commonest.
  • Other sources: spread from skin, lachrymal ducts, middle ear etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

examiantion for pre-septal vs orbital (more serious) cellulitis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

management of pre-orbital sepsis

A
  • Admit.
  • IV access.
  • FBC/CRP, cultures.
  • Nose swab.
  • IV Ceftriaxone.
  • ± IV Metronidazole
  • (if sinuses involved)
  • Prompt ENT and
    Ophthalmology
    review.
  • 4h obs.
  • Consider CT scan.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

pneumonia differentials

A
  • Bronchiolitis (Viral CAP). * Pertussis.
  • Heart failure.
  • Sepsis.
  • Metabolic acidosis.
  • Non-infectious mimics.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

pneumonia differentials

A
  • Bronchiolitis (Viral CAP). * Pertussis.
  • Heart failure.
  • Sepsis.
  • Metabolic acidosis.
  • Non-infectious mimics.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

signs of pneumonia

A

fine crackles
bronchial breathing
reduced air entry
wheeze

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Fine crackles:

A
  • Short, explosive, non-musical sounds.
  • Heard during mid-to-late inspiration.
  • Sounds like Velcro being gently separated.
  • Made by sudden opening of small airways.
  • NOT affected by coughing.
  • Also heard in: pulmonary fibrosis.
    heart failure.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Bronchial breathing:

A

Bronchial breathing:
* Heard in both phases of respiration.
* Sounds like tracheal sounds.
* Indicates airway surrounded by consolidated
lung tissue – transmitting sound to surface.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Reduced air entry.
.

A
  • Consolidation with embedded airways blocked by inflammation or secretions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Wheeze:

A
  • High-pitched usually expiratory sound.
  • Suggests airway narrowing.
  • Can be present in pneumonia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

investigations severity assessment for pneumonia

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

bacterial vs viral caap presentation

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

management of CAP

A

ALL suspected bacterial CAP need antibiotics

Oral for moderate CAP unless can’t tolerate.

IV for severe/complicate ± moderate.

Duration depends on severity and response.
- Non-severe: Amoxicillin ± Clarithromycin.
- Severe: Co-amoxiclav ± Clarithromycin.
-or- Cefuroxime ± Metronidazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

define Brief Resolved Unexplained Event BRUE - formerly acute life-threatening event

A

A sudden, brief, now resolved episode in an infant with:

  • Cyanosis or pallor,
  • Absent, decreased or irregular breathing,
  • Marked changes in tone (hypo- or hyper-tonia),
  • Altered level of consciousness
    Applies only when no other explanation after assessment
    1. Brief = <1 minute.
    2. Now resolved = infant asymptomatic on presentation.
    3. 3. With = 1 or more criteria.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

BRUE risk screening for discharge

A
  • Age >60 days
  • If premature: born at gestational age >32 weeks and
    current postconceptional age >45 wks.
  • Only 1 BRUE (NO prior BRUE i.e., first event).
  • Duration of BRUE <1 minute.
  • NO CPR required by trained medical care provider.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

low risk BRUE management

A
  • Educate caregiver; offer CPR training.
  • ± ECG and O/N monitoring.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

high risk BRUE management

A
  • Admit for continuous oximetry observation.
  • ECG.
  • FBC, bicarbonate, glucose, metabolic screen.
  • Blood and urine culture.
  • Respiratory virus testing; Pertussis testing.
  • Observe/evaluate feeding.
  • Prescribe anti-reflux medication.
  • Home monitoring.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Asthamtic history

A
  • Acuity of onset?
  • Potential trigger - recent URTI? allergen exposure?

Background asthma history?

  • Regular asthma medication.
  • Frequency of preventer use.
  • Frequency of/last course of oral steroids.
  • Previous ED and GP attendances.
  • Social impact – days off school.

Risk of severe asthma?

  • Repeated ED attendance esp. In last year.
  • Previous admissions, esp. in last year.
  • Previous near fatal asthma (ICU admission).
  • Pulse and respiratory rates; SpO2 in air.
  • Work of breathing – use of accessory muscles.
  • Breath sounds – unequal, silent chest?
  • Amount of wheeze.

**Other causes/complications? **

  • Pneumonia
  • Pneumothorax.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

assessment of asthma severity

A
40
Q

management of acute asthma exacerbation

A
41
Q

history for croup

A
  • Acuity of onset?
  • Any preceding symptoms: runny nose; fever?
  • Other symptoms:
    Toxicity (very high To). Choking episode/trigger. Drooling.
    Voice changes/hoarseness. Cyanotic episodes.
  • Vaccinationstatus?
  • Abnormal respiratory sounds/stridor.
  • Respiratory status – RR; WOB.
42
Q

what is croup

A

common (>95%) cause of laryngotracheal infections

  • Typically occurs between 6mo and 6yr (peak 2yr).
43
Q

aetiology of croup

A

Parainfluenza virus (commonest).
Influenza virus, RSV, Adenovirus. Measles.

44
Q

presentation of croup

A

hoarse voice.
barking cough. stridor.
± fever.

45
Q

differential for croup

A
46
Q

stridor, stertor or wheeze

A
47
Q

scoring croup

A

Westley croup severity score

48
Q

management of croup accoridng to Westley severity

A
49
Q

epiglottitis

A

Epiglottitis is inflammation and swelling of the epiglottis. It’s often caused by an infection, but can also sometimes happen as a result of a throat injury. The epiglottis is a flap of tissue that sits beneath the tongue at the back of the throat.

50
Q

aetiology of epiglorttiis

A

Epiglottitis is inflammation and swelling of the epiglottis. It’s often caused by an infection, but can also sometimes happen as a result of a throat injury. The epiglottis is a flap of tissue that sits beneath the tongue at the back of the throat.

51
Q

clinical presentation of epiglottitis

A

.

52
Q

children with epiglottiis may sit in a certain position

A
53
Q

management of epiglottitis

A

1) Secure the airway
2) Give oxygen if sats <92%
3) IV antibiotics (e.g. ceftriaxone)
4) Steroids (i.e. dexamethasone)

54
Q

sickle cell

A
  • Autosomal recessive inheritance.
  • Commonly in black and Afro-Caribbean people
55
Q

natural hisotry of sickle cell disease

A

Common factor in distribution is history of malaria or migration from a malaria area.
* Carrier offers protection against malaria.

56
Q

sickle cell disease pathophysiology

A
  • Mutation in the Beta-globin gene.
  • Changes 6th amino-acid - glutamine to valine.
  • HbS is insoluble when deoxygenated forming * polymers which damage red cell membranes.
  • Results in rigid sickle shaped cells which tend * to cause vaso-occlusion; causes cascade of
  • pathological events: Infarction, vasculopathy, * haemolysis, inflammation.
57
Q

acute clinical manifestatins of sickle cell

A

anaemia
acure anaemia
infection
painful crises
priapism

58
Q

Infection in Sickle cell disease?

A
59
Q

longterm problems in sickle cell disease

A
60
Q

investigations for sickle cell

A
61
Q

when to admit to hospital : sickle cell

A
62
Q

management principles for sickle cell diagnosis

A
  • Oxygenation.
  • Pain relief (within 30 minutes).
  • Fluid replacement (PO or IV):
  • Reduced tubular concentrating.
  • High viscosity worse sickling.
  • Red cell transfusion (urgent)
  • Broad spectrum antibiotics.
63
Q

key points about sickle cell disease

A
64
Q

meningitis history and examination

A
  • Acuity of onset?
  • Any recent infection e.g. viral URTI/herpes?
  • Altered behaviour:
  • drowsiness/lethargy
  • irritability, confusion
  • Poor feeding/off feeds; vomiting?
  • Photophobia? * Seizures?
  • Full/bulging fontanelle (<18 months).
  • Neck stiffness, +ve Brudzinski/Kernig signs.
  • Focal neurological signs/papilloedema.
65
Q

differential diagnosis for meningitis

A
  • Bacterialmeningitis.
  • Viral meningitis.
  • Viral encephalitis.
  • Tuberculous meningitis.
  • Cerebral abscess.
  • Hydrocephalus.
  • Non-accidental injury.
66
Q

bacterial meningitis ABCDE assessment

A
67
Q

management of bacterial meningitis

A

Sepsis 6
Lumbar puncture

68
Q

lumbar puncture contraindications

A
69
Q

Typical changes in the CSF in meningitis or encephalitis

A
70
Q

Acute management of bacterial meningitis

A
71
Q

complications of bacterial meningitis

A
72
Q

meningococcal septicaemia aetiology

A

VERY HIGH RISK OF MORTALITY
- 12 capsular serotypes; commonest in UK (B,C, W, Y).
- Carried in nasopharynx:
- rate low in infants/young children.
- 25% of adolescents.
- 5-11% of adults.
- 5-11% of adults.
- Droplet spread; needs prolonged close contact.
- Not understood why disease develops in some individuals.

73
Q

presentation of meningococcal septicaemia

A
  • incubation period of 2-7 days. Prodrome: coryzal (‘flu-like’) illness.
  • fever.
  • poor feeding, vomiting, diarrhoea. headache, irritable, drowsy, seizures.
  • Rash present in only 80% at presentation.
74
Q

risk factors of meningococal carries becoming unwell

A

Age, season (Winter), smoking.
Preceding Influenza A infection.
Living in ‘closed’/’semi-closed’ community.

75
Q

is meningococcal meningitis the same as meningococcaemia

A

Meningitis can occur with/without septicaemia Septicaemia can occur with/without meningitis

76
Q

management of meningococcal septicaemia

A
77
Q

common causes of seziures

A
  • Febrile convulsions
  • Known epilepsy ± acute illness
  • Meningitis or encephalitis
  • Hypoglycaemia/hypocalcaemia
  • Metabolic/Poisoning
  • Trauma – accidental or non-accidental
78
Q

Febrile convulsion

A
  • 6 months to 5 years – no prev. neurology.
  • Generalised in nature.
  • Less than 15 minutes duration.
  • No IC infection/metabolic disturbance.
  • Simple or complex.
  • Recurrence risk 30-40%.
79
Q

Infantile spasms

A
  • Age of onset: 3-12 months.
  • Sudden violent flexor spasms of head, trunk
    and limbs followed by extension of arms.
  • Last 1-2 seconds; occur multiple/day.
  • Often with developmental regression.
  • EEG: hypsarrthymia; Rx ACTH, steroids.
80
Q

Absence Epilepsy

A
  • Age of onset: 4-12 years; girls>boys.
  • Sudden onset; last few seconds (<30).
  • Associated with automatisms – flickering of
    eyes, purposeless movement of eyes/mouth.
  • EEG: 3 per second (hz) spike and wave.
  • Spontaneous remission in adolescence.
81
Q

investigations for seizure

A
82
Q

managment of a seizure

A

1) ABCDE (DONT EVER FORGET GLUCOSE)

10 mins
2) Benzodiazepine
- IV/ IOacces- Lorazepam
- no IV access- Midazolam (buccal), diazepam (rectal)

10mins
Still fitting?

3) Lorazepaman IV

+- Paraldehyde PR

10 mins
Still fitting?

4) Phenytoin IV/IO Phenobarbitone IV/IO

Still fitting?

5) Rapid sequence induction (RSI) with thiopentone to ge thold of airway

after 30 mins = Status epilepticus

83
Q

Status epilepticus

A

A seizure that lasts longer than 5 minutes, or having more than 1 seizure within a 5 minutes period, without returning to a normal level of consciousness between episodes is called status epilepticus

84
Q

differentials: 6-year-old boy presents to ED with a fever and an acute antalgic gait.

A
  • Transient synovitis.
  • Septic arthritis.
  • Osteomyelitis.
  • Trauma; non-accidental injury.
  • Malignancy (leukaemia,neuroblastoma).
  • Perthes disease.
  • Juvenile idiopathic arthritis.
85
Q

presentation of septic arthritis

A
86
Q

investigations for septic arthritis

A
87
Q

management of septic arthritis

A
88
Q

Atraumatic limp summary

A
89
Q

clinical presentations of dehydration e.g. due to sickness and diarrhoea

A
90
Q

history, examination and investigations for dehydration

A
  • Onset, frequency (stools/vomits), duration.
  • Number times urinated in past 24 hours.
  • Risk factors for dehydration?
  • Other family members/contacts unwell?
  • Recent foreign travel?
  • Consumption of unsafe foods - takeaway, BBQ?
  • Clinical evidence of dehydration
  • Features suggestive of hypernatraemia
91
Q

risk factors for dehydration

A
  • <1 year old, especially <6 months old
  • Low birth weight
  • Signs of malnutrition
  • Stopped breastfeeding during illness
  • Not offered/not tolerated fluids before
    presenting
  • > 5 episodes of diarrhoea in past 24h – or –
  • > 2 vomits in past 24h
92
Q

managment of dehydration based on severity

A
93
Q

presentation of DKA

A

Early:
Most common – the ‘classical triad’:
* Thirst (excessive drinking/polydipsia).
* Polyuria.
* Weight loss (over short period of time).
Less common:
* Fatigue.
* Enuresis (secondary).
* Polyphagia (excess hunger/eating). * Recurrent infections (e.g., candida)
Late (diabetic ketoacidosis):
* Smell of ketones.
* Nausea and vomiting.
* Dehydration.
* Hyperventilation due to acidosis.
* Abdominal pain.
* Drowsiness.
* Hypovolaemic shock.
* Coma and death.

94
Q

criteria for diagnosiing T1DM

A
95
Q

Pathophysiology of Diabetic Ketoacidosis

A
96
Q

management of DKA

A
97
Q

types of insulin

A

Paediatrics (Y4) (42 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions