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Phase 3a Medicine Sheffield > Paediatrics > Flashcards

Paediatrics Flashcards

1
Q

What are some common viral causes of resp infections?

A
  • RSV (respiratory syncytial virus
  • Rhinovirus
  • Influenza
  • Metapneumovirus
  • Adenovirus
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2
Q

What are some common bacterial causes of resp infections?

A
  • Mycoplasma pneumoniae
  • Bordetella pertussis
  • Moraxella catarrhalis
  • Haemophilus Influenza
  • Strep Pneumonia
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3
Q

What are some risk factors for resp infections?

A
  • Parental smoking
  • Poor socioeconomic status
  • Poor nutrition
  • Male
  • Immunodeficiency
  • Underlying condition
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4
Q

Give 3 URTis and state what they can cause.

A

URTis and what they cause

  • Coryza (cold)
  • Sore throat (pharyngitis, tonsillitis)
  • Acute otitis Media
  • Sinusitis

Causes

  • Difficulty feeding
  • Febrile convulsions
  • Asthma exacerbations
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5
Q

What is the Centor Criteria?

A

Set of Criteria to determine the likelihood of a sore throat being bacterial.

  • Tonsillar exudate
  • Tender anterior cervical lymphadenopathy
  • Fever
  • Absence of cough

3+ = Strep infection needing Abx

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6
Q

What is Whooping Cough?

A

Acute highly contagious resp infection transmitted by resp droplets . Co-infection with RSV is common.

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7
Q

What is the cause of Whooping Cough?

A

Caused by Bordetella pertussis, gram neg coccobacillus cultured on bordet gengou agar.

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8
Q

How long do symptoms last and what are the two stages of Pertussis?

A

Symptoms last 6-8 weeks.

Catarrhal stage
Paroxysmal coughing

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9
Q

What are the symptoms in the catarrhal stage?

A
  • Malaise
  • Conjunctivitis
  • Nasal discharge
  • Sore throat
  • Dry cough
  • Mild fever
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10
Q

What are the symptoms in the paroxysmal coughing stage?

A

Dry hacking cough that is worse at night and after feeding

Coughing followed by the characteristic whoop - inspiration against the closed epiglottis.

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11
Q

What can be complications of whooping cough?

A

Post cough – vomiting, apnoea,cyanosis

Subconjunctival haemorrhage/anoxia can be brought on by coughing fits  seizures and syncope

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12
Q

What investigations would be appropriate in Whooping cough?

A
  • PCR via nasal swabs
  • Lymphocytosis common
  • Nasopharyngeal swabs
  • Test for anti-pertussis IgG
  • Culture is the gold standard.
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13
Q

What is the management of Whooping Cough?

A

Hospitalised if over 6 months –> risk of apnoea
10-14 days incubation

Marcolides 1st line - Azithromycin or clarithromycin or erythromycin

Erythromycin for pregnant women

Off school for 48 hrs after Abx start

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14
Q

What is Acute Epiglottitis?

A

Life threatening emergency due to high risk of resp obstruction.

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15
Q

What is the cause of Acute Epiglottitis?

A

Haemophilus influenza Type B (Hib)

Hib immunisation - 99% reduction in cases, most common in ages 2-7yrs

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16
Q

What are the symptoms of Acute Epiglottitis?

A 
Intense swelling of epiglottis 
Very acute onset
Drooling
Stridor
High fever
Dysphagia and speech difficulty due to pain 
Minimal cough
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17
Q

What investigations should be ordered for acute epiglottitis?

A
  • Laryngoscopy
  • Lateral neck x-ray
  • FBC
  • Blood cultures/swab of epiglottis.
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18
Q

What should you never do when suspecting an obstruction of the resp tract/acute epigglottits?

A

Do not upset or cannulate

Do not examine throat with spatula or lie them down.

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19
Q

What is Croup?

A

Laryngotracheobronchitis.

Mucosal inflammation and increased secretions that affect the airway. Can cause dangerous oedema in the subglottic area which may narrow the trachea.

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20
Q

What are some viral causes of croup?

A

Parainfluenza 1,2,3 (most common)
RSV
Influenza
Metapneumovirus

Most common in the autumn time – 6 months to 6yrs with a peak incidence at 2yrs.

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21
Q

How does Croup present?

A
  • Barking cough (worse at night)
  • Harsh stridor
  • Hoarseness
  • Preceding nonspecific viral URTI
  • Coryza, fever, cough
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22
Q

What are some signs of severe Croup?

A
  • Cyanosis
  • Rising HR/RR
  • Restlessness
  • Altered consciousness
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23
Q

What investigations can diagnose Croup?

A

Most diagnosed clinically

X-ray signs –> Posterior-anterior view = subglottic narrowing = steeple sign

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24
Q

How should you manage Croup?

A

CKS recommend giving a single dose of oral dexamethasone (0.15mg/kg) to all children regardless of severity

Prednisolone is an alternative if dexamethasone is not available

Emergency – high flow oxygen + nebulised adrenaline.

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25
Q

When should a child be admitted to hospital?

A

Should be admitted if they have mod/severe croup. Other factors include if they are less than 6months old or have known upper airway abnormalities.

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26
Q

What is Bacterial Tracheitis?

A

Inflammation of the Trachea due to a bacterial infection.

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27
Q

How does Bacterial Tracheitis present?

A

Pseudomembranous croup – uncommon but very similar to severe croup but presents with

High fever 
Appears toxic
Tracheal tenderness 
Rapidly progressive airway obstruction – can’t be cleared by coughing 
Severe stridor
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28
Q

What is the cause of Bacterial Tracheitis?

A

S aureus, strep A, haemophilus

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29
Q

What investigations should be ordered in bacterial tracheitis?

A

Requires direct vision of exudates or pseudo membranes on trachea

X-ray indicates subglottic narrowing

FBC/WCC/ESR

Blood cultures

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30
Q

How should you treat Bacterial Tracheitis?

A

Stabilise airway

Treat with IV abx

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31
Q

How would a child with a tracheal obstruction be?

A

immobile, upright with an open mouth to optimise airway.

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32
Q

What is the common cold?

A

Viral URT affecting the nose, throat, sinuses and larynx.

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33
Q

What are some symptoms of the common cold?

A
  • Clear/ mucopurulent nasal discharge and blockage
  • Coughing
  • Headache
  • Sneezing
  • Fever
  • Sore throat.
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34
Q

What are some common pathogens that cause the common cold?

A
  • Rhinoviruses
  • Coronaviruses
  • RSV
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35
Q

What is the treatment of the common cold?

A
  • Paracetamol

- Ibuprofen

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36
Q

What is the management of Acute Epiglottitis?

A

IV Abx – fetotaxime
Intubate
Tracheostomy may be needed if complete obstruction

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37
Q

What is Tonsilitis?

A

Form of pharyngitis where there is intense inflammation of the tonsils with often purulent exudate.

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38
Q

What are the symptoms of Tonsilitis?

A
  • Sore throat/ scratchy voice/ Dysphagia
  • White or yellow coating/patches on the tonsils
  • Fever
  • Red swollen tonsils
  • Lymphadenopathy in the neck
  • Bad breath
  • Stomach ache/headache
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39
Q

Give 2 risk factors of Tonsilitis?

A

young age and frequent exposure to germs

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40
Q

What are the causes of tonsilitis?

A
  • Group a beta-haemolytic strep

- Contact with infected people

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41
Q

What investigations should you order in tonsilitis?

A
  • Throat culture
  • Rapid streptococcal antigen test
  • WBC
  • Serological testing for streptococci
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42
Q

What is a complication of Tonsilitis?

A

Quinsy - Peritonsillar abscess

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43
Q

What are the symptoms of Quinsy?

A

Sore throat, dysphagia, uvula deviation, trismus (lockjaw)

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44
Q

What is Toxoplasmosis?

A

Disease from infection of toxoplasma gondii parasite.

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45
Q

What are the causes of Toxoplasmosis?

A
  • Infected cat faeces
  • Raw Meat
  • Mother to child transmission
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46
Q

What are the symptoms of Toxoplasmosis?

A

Causes microcephaly, fits and sensorineural deafness

Eye infections

Headaches, confusion.

Flu like symptoms in most people –> headache, fever, fatigue, aches

Signs –> Cerebral calcification, microcephaly/hydrocephaly, chorioretinitis, cerebral palsy.

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47
Q

What investigations should be ordered to diagnose toxoplasmosis?

A

Diagnosed by serology –>95% asymptomatic

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48
Q

How should you treat toxoplasmosis?

A

Pyrimethamine
Sulphadiazine
Spiramycin

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49
Q

What is Rubella?

A

Notifiable disease.

An RNA virus (Rubivirus togaviridae) transmitted as droplets with an incubation period of 14-21 days.

Infectious for up to 5 days before and 5 days after start of rash

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50
Q

What is the prodrome/symptoms of Rubella?

A
  • Lethargy
  • Low grade fever (less than 38.9)
  • Headache
  • Mild conjunctivitis
  • Anorexia
  • Rash
  • Aching joints – especially in women.
  • Suboccipital lymphadenopathy
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51
Q

What is the rash like?

A

Initially pink discrete macular rash that coalesce starting behind the ear and face then spreading the entire body.

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52
Q

What are some differential diagnoses of Rubella?

A
  • Contact dermatitis
  • Erythema multiforme/drug allergy
  • Measles
  • Scarlet fever
  • Kawasaki disease
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53
Q

What are the diagnostic tests for Rubella?

A

PCR testing

FBC shows low WBC with increased proportion of Lymphocytes and thrombocytopenia

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54
Q

What is the treatment for Rubella?

A

Vaccine
Antipyretics for fever

Pregnant women may be given hyperimmune globulin if they continue their pregnancy.

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55
Q

What can Rubella do to the development of a foetus in the following periods?

1-4 weeks
4-8 weeks
8-12 weeks

A

1-4 weeks - eye anomaly (70%)
4-8 weeks - cardiac abnormality (40%)
8-12 weeks - deafness (30%)

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56
Q

What is Measles?

A

Notifiable disease

Acute viral infection caused by single stranded RNA morbillivirus from the paramyxovirus family

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57
Q

What is the incubation period of measles?

How long is the person infectious for?

A

Incubation period of 7-12 days and spread through resp droplets

Infectious from prodrome until 4 days after the rash of measles appear.

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58
Q

What are the risk factors of Measles?

A

travelling internationally, being unvaccinated, Vit A deficiency (worse complications)

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59
Q

What are the differential diagnoses of Measles?

A

Rubella, Parvovirus B19, Enterovirus, Scarlet fever

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60
Q

What is the prodrome of Measles?

A

Days of the 4 C’s - Cough, Coryza, Conjuncitivits, Cranky

+ Koplik’s spot on palate – small red spots each with a bluish white speck in the centre

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61
Q

What is the clinical presentation of measles?

A

Rash for at least 3 days

Fever for at least one day (often over 40) and at least one of
o Cough
o Corzya
o Conjunctivitis

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62
Q

What is the Measles Rash like?

A

First seen on forehead, neck and behind ears, spreads to limb/trunk over ¾ days and then fades after 3-4 days and leaves behind brown discolouration.

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63
Q

What is the diagnostic tests for measles?

A
  • Igm + IgG positive
  • Salivary swab or serum sample for measles specific immunoglobulin taken within 6 weeks of onset
  • RNA detection in salivary swabs
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64
Q

What are some complications of Measles?

A

More common if <5 yrs or >20 years

Otitis media
Croup/tracheitis
Pneumonia – most common cause of measles death
Encephalitis/pneumonia in older patients

Pregnancy – Increased risk of miscarriage, prematurity and low birth weight.

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65
Q

What is the treatment for Measles?

A

Paracetamol/ibuprofen and fluids

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66
Q

What is encephalitis?

A

Inflammation of the Brain.

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67
Q

What are some infective causes of encephalitis?

A

HSV, Mumps, varicella zoster, rabies, parvovirus, immunocompromised, influenza, TB, Toxoplasmosis, and malaria

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68
Q

What are some of the clinical signs of encephalitis?

A
  • Flu like prodrome
  • Reduced consciousness
  • Change in behaviour
  • Vomiting
  • Fits/seizures
  • Fever/lethargy
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69
Q

What investigations should you order for encephalitis?

A
  • LP, PCR
  • Bloods
  • Stool for enteroviruses
  • Urine
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70
Q

What does a LP look like in Encephalitis?

A
  • Lymphocytosis
  • Raised protein
  • Normal glucose
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71
Q

What is the management of Encephalitis?

A

HSE – Herpes simplex encephalitis – most treatable – acyclovir

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72
Q

What is Kawasaki’s disease?

A

Idiopathic systemic vasculitis that most commonly effects children between 6 months and 5 years

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73
Q

What is a major complication of Kawasakis disease?

A

Coronary Artery Aneurysm

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74
Q

What is the Clinical Presentation of Kawasaki’s disease?

A

MyHEART

Mucosal involvement – inflamed dry lips/strawberry tongue

Hand and feet swelling 
Eyes – bilateral conjuctivits 
Lymphadenopathy (cervical)
Rash
Temp – >5 days of fever
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75
Q

What are the 3 phases of Kawasaki’s disease?

A

Acute febrile 1-2 weeks
- Fever + 4 of criteria (MyHEART)

Subacute – remission of fever (4-6 weeks)
- Development of Coronary artery aneurysms

Convalescent (6-12 weeks)
- Resolution of clinical signs + normalisation of inflammatory markers

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76
Q

What is the differential diagnosis of Kawasaki’s disease?

A
  • Measles, Rubella, Parvovirus B19
  • Infectious mononucleosis/glandular fever
  • Scarlet Fever
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77
Q

What investigations should you order for Kawasakis disease?

A
  • Increased ESR + CRP
  • WWC
  • Platelets
  • AST
  • A1-Antitrypsin
  • Bilirubin
    Echo is essential to reveal dilation and aneurysms of coronary arteries.
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78
Q

What is the management of Kawasaki’s disease?

A

Aspirin
IV immunoglobulins

Treatment is to reduce the risk of aneurysms and thrombosis, follow up echo 6 weeks later to check for aneurysms.

Treatment for permanent inflammation –> Infliximab (anti-TNF)

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79
Q

What is Chicken Pox?

A

Highly infectious disease caused by varicella zoster (VZV)

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80
Q

What can VZV reactivation cause in adults?

A

Reaction of VZV leads to herpes zoster (shingles) in the posterior root ganglia.

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81
Q

What are some of the risk factors for chicken pox?

A

Immunocompromised, Older age, Steroid use, Malignancy

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82
Q

What is the pathophysiology of Chicken Pox?

A

Virus enters through URT  viraemia after 4-6 days

Infective from 4 days prior to rash until all lesions have scabbed (day 5)

Droplet spread - 95% of adults have been infected and immunity is life long

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83
Q

What is the clinical presentation of Chicken Pox?

A

Temp 38-39
Headache,malaise
Crops of vesicles (itchy)

Vesicles are usually found on the head, neck and trunk, very sparse on the limbs

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84
Q

What is the cycle of a vesicle?

A
  1. Macule
  2. Papule
  3. Vesicle
  4. Ulcer
  5. Crust
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85
Q

In chickenpox what does redness around a lesion indicate?

A

Redness around the lesion suggests bacterial superinfection

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86
Q

What are some of the differential diagnoses of chicken pox?

A

Shingles – only one dermatome Patient with vesicles at different stages of evolution in one dermatome distribution

Generalized herpes zoster/simplex

Dermatitis herpetiformis

Impetigo

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87
Q

What are the diagnostic tests for chicken pox?

A

Clinical – fluorescent antibody tests – for IgM and IgG

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88
Q

What are some complications of chicken pox?

A
  • Pneumonia
  • Encephalitis
  • Dissemiated haemorrhage chickenpox
  • Secondary bacterial infection of the lesions
  • Arthritis, nephritis, pancreatitis
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89
Q

What is the appropriate management for Chickenpox?

A
  • Calamine lotion
  • Antivaricella – zoister immunoglobulin
  • Acyclovir (If severe/at risk of complications)
  • Flucloxacillin in bacterial superinfection
  • 5 days off school for kids
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90
Q

What is anaphylaxis?

A

Severe life threatening hypersensitivity reaction of sudden onset

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91
Q

What may anaphylaxis be brought on by?

A
  • Foods
  • Insect sting
  • Drugs
  • Latex
  • Exercise
  • Inhaled allergens

Nuts is the main cause in adults.

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92
Q

What are the symptoms of anaphylaxis?

A

Skin reactions – hives, itching and flushed or pale skin.

Hypotension and a weak rapid pulse.

Constriction of airways and a swollen tongue or throat - wheeze and difficulty breathing.

N+V/diarrhoea.

Dizziness or fainting.

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93
Q

What is the management of anaphylaxis?

A

ABCDE

IM Adrenaline

  • Under 6 months – 0.15mg
  • 6 months to 6 years – 0.15mg
  • 6-12 Years – 0.3mg
  • Over 12 years – 0.5mg
Antihistamine
Hydrocortisone 
Salbutamol if wheeze
High flow O2 and IV fluids 
Monitor pulse oximetry, ECG and BP
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94
Q

What investigations could confirm anaphylaxis?

A

Clinical symptoms + presentation

Serum tryptase levels can remain elevated for up to 12 hrs after an attack.

95
Q

What investigations can be used to diagnose anaphylaxis?

A

Clinical symptoms + presentation

Serum tryptase levels can remain elevated for up to 12 hrs after an attack.

96
Q

What is Scarlet Fever?

A

Notifiable disease – endotoxin mediated disease arising from a bacterial infection by an erythrogenic toxin producing strain of –> Strep pyogenes – group A haemolytic streptococci

97
Q

What is the epidemiology of scarlet fever?

A

87% under 10 years old and unusual under 2 years.

98
Q

What is the prodrome for scarlet fever?

A
  • Sore throat + tonsillitis
  • Fever
  • Headache
  • Vomiting and abdo pain
  • Myalgia
99
Q

What is the clinical presentation of scarlet fever?

A
  • Strawberry tongue
  • Acute onset sore throat and ever then rash 24-48 hours after
  • Scarlatiniform rash – typically appears first on chest, axilla and behind ears
    o Later on the trunk and legs
  • Around the mouth (circumoral)
100
Q

What is the rash like in Scarlet fever?

A

Red, pin prick blanching rash which is Sandpaper/rough like

101
Q

What are some differential diagnoses for scarlet fever?

A
  • Other viral exanthema
  • Infectious mononucleosis (often cause is ebv)
  • Toxic shock syndrome
  • Kawasaki disease
102
Q

What investigations can be diagnostic in scarlet fever?

A

Clinical features

Throat swab - should be taken but antibiotic treatment not delayed

Antigen detection kits

Strep antibody tests

103
Q

What are some of the complications caused by scarlet fever?

A
  • Syndehnhams chorea
  • Ottits media
  • Rheumatic fever
  • Glomerulonephritis
104
Q

What is the treatment for Scarlet Fever?

A

Penicillin/azithromycin (if allergic) for 10 days then rest fluids para/ibuprofen

Can return to school 24 hours after starting abx.

105
Q

What is Coxsackie’s disease (Hand foot and mouth)?

A

Viral illness commonly causing lesions involving the hands, feet, and mouth.

Transmitted faeco-orally.

106
Q

What is the cause of? Coxsackie’s disease?

A

Coxsackievirus A16 and Enterovirus 71

107
Q

What is the epidemiology of Coxsackie’s disease?

A

Common in infants younger than 10 - outbreak common in nurseries, schools and childcare settings

108
Q

What is the prodrome of Coxsackie’s disease?

A
  • Fever
  • Malaise
  • Loss of appetite
  • Sore mouth/throat
  • Cough
  • Abdo pain
109
Q

What are the mouth lesions like in Coxsackie’s disease?

A

On buccal mucosa, tongue, or hard palate

Begin as macular lesions that progress to vesicles which then erode

Yellow ulcers surrounded by red haloes

110
Q

What are the skin lesions like in Coxsackie’s disease?

A

Palm, soles and between fingers and toes

Erythematous macules but rapidly progress to grey vesicles with an erythematous base

Can also appear on trunk, thighs, buttocks and genitalia

111
Q

What are some of the differential diagnoses of Coxsackie’s disease?

A
  • Herpes simplex/zoster
  • Chicken pox
  • Kawasaki’s disease
112
Q

What are the investigations for diagnosing Coxsackies disease?

A
  • PCR
  • Clinical diagnosis
  • Swab of lesions
113
Q

What is the management of Coxsackie’s disease?

A
  • Fluid intake, soft diet + para/ibuprofen
  • If mouth is very painful, topic agents e.g. lidocaine oral gel
  • Stay off school until better
114
Q

What is Turner’s syndrome?

A

Chromosomal disorder affecting 1 in 2500 females, caused by the presence of only one X chromosome or the deletion of the short arm in one of the X chromosomes.

115
Q

What happens to females with Turners syndrome?

A

Almost all affected infertile and many girls experience short stature and ovarian failure

116
Q

What does Turners syndrome increase the risk of?

A
  • CHD
  • Renal malformations
  • Hearing loss
  • Osteoporosis
  • Obesity
  • Diabetes
  • Atherogenic lipid profile
117
Q

Turners Syndrome

What is the clinical presentation of a newborn?

A
  • Lymphoedema
  • Cardiac/renal abnormalities
  • Coarctation, absence of kidney
118
Q

Turners Syndrome

What is the clinical presentation of an infant?

A

Short stature, webbed neck

Broad chest/widely spaced nipples

Bicuspid aortic valve 15% and coarctation of the aorta 10%

High arched palate

Recurrent otitis media/hearing loss

Behavioural issues

119
Q

Turners Syndrome

What is the clinical presentation of an adolescent?

A
  • Gonodal dysgenesis
  • Absent/incomplete puberty
  • Amenorrhoea
  • Impaired growth
120
Q

What AI conditions is Turners syndrome associated with?

A

Thyroid, Diabetes, Coeliac, Crohns

121
Q

What are the diagnostic tests for Turners syndrome?

A

Can be diagnosed by amniocentesis or Chorionic villous sampling

Chromosomal analysis

122
Q

What is the treatment for Turners Syndrome?

A

Treat complications and monitor AI associations

Short stature – recombinant Human growth hormone

Oestrogen (12years) to initiate puberty and prevent osteoporosis

123
Q

What is Prader Willi Syndrome?

A

First human disorder attributed to genomic imprinting. Usually caused by a deletion in a paternal gene, opposite to Angelman’s.

124
Q

What are some of the Key Features seen in Prader Willi, what would you expect to see in infancy and in adolescence?

A

Key Features - hypotonia, hypogonadism, obesity/hyperphagia.

Infant – hypotonia and development delay

Adolescence – obesity, learning and behavioural difficulties especially with food

125
Q

What is the cause of Prader Willi Syndrome?

A

Absence of the active Prader Willi gene on the longarm of chromosome 15

—> Deletion in the paternally inherited chromosome 15 (70%) or maternal uniparental disomy 15

126
Q

What is the infant presentation of Prader Willi Syndrome?

A
  • Usually, blue eyes blond hair
  • Hypotonia at birth
  • Failure to thrive
  • Genital hypoplasia
  • Delayed motor milestones
127
Q

What is the adolescent presentation of Prader Willi Syndrome?

A
  • Hyperphagia – always hungry  obesity
  • Short stature
  • Behavioural issues
  • Low IQ

Usually have hyperphagia due to elevated levels of ghrelin

128
Q

What is the treatment of Prader Willi Syndrome?

A
  • Growth hormone
  • Anti-psychotics – olanzapine, haloperidol
  • Fluoxetine and SSRI’s are sometimes effective
129
Q

What is Angelmans syndrome and how is it caused?

A

Genetic imprinting disorder due to maternal deletion of chromosome 15

Opposite to Prader Willi

130
Q

What is the clinical presentation of Angelmans syndrome?

A
  • Developmental delay
  • Motor milestones delayed
  • Speech impairment
  • Behavioural signs
  • Ataxia
  • Strabismus
  • Drooling
  • Fascination with water
  • Epilepsy 90%
  • Microcephaly
131
Q

What are the behavioural signs of angelmans syndrome?

A
  • Short attention span
  • Laughter and happiness/excited
  • Laughs at most stimuli
  • Hand flapping common
  • Tendency to pinch/grab/bite
  • Fascination with water
132
Q

What are the facial features of Angelmans syndrome?

A
  • Microcephaly
  • Flat occiput
  • Prominent mandible
  • Wide mouth
  • Wide space teeth
  • Drooling/tongue thrusting
133
Q

How is the diagnosis of Angelmans syndrome made?

A

Chromosomal analysis

V similar to autism

Fluorescence in situ hybridisation (FISH) - detects 80-85% of all deletions

134
Q

What is the appropriate treatment of Angelmans syndrome?

A 
Behavioural modification programmes
Speech therapy 
Physiotherapy
Parental education 
Anti-convulsant for epilepsy – valproate/clonazepam
135
Q

What is Sinusitis?

A

Inflammation of the mucous membranes of the paranasal sinuses.

136
Q

What is the usual causes of Sinusitis?

A

Most common infectious agents – Streptococcus pneumoniae, Haemophilus Influenzae and rhinoviruses

137
Q

What are the features in Sinusitis?

A

Facial Pain –> typically frontal pressure pain which is worse when bending forward

Nasal discharge – usually thick and purulent

Nasal Obstruction

Pyrexia

138
Q

How would you normally diagnose Sinusitis?

A

Normally just clinical examination/features

Allergy testing may be done if the aetiology is believed to be allergies.

Imaging not common but CT will show the sinuses.

139
Q

What is the appropriate management of Sinusitis and how is most of it managed?

A

Treat conservatively with mild analgesia like paracetamol +ibuprofen

Intranasal corticosteroids to be considered if symptoms present for over 10 days.

Oral antibiotics not usually required but may be given if severe
o First line – phenoxymethylpenicillin
o Or Co-Amoxiclav if very systemically unwell

Avoid antihistamines as they may thicken secretions

140
Q

What is Erythema Infectiosum?

A

Slapped Cheek Syndrome

141
Q

What are the prodrome symptoms of erythema infectiosum and how long do they last for?

A

They last around a week:

Mild
Headache rhinitis, sore throat, fever, malaise
Then 1 week of symptom free

142
Q

What follows the prodrome of Erythema Infectiosum?

A

7-10 days of no symptoms after prodrome

Classic slapped cheek rash

1-4 days after facial rash, erythematous macular morbilliform rash develops on the limbs

Arthralgia

143
Q

What is the differential diagnosis of Erythema Infectiosum?

A

Rubella
Measles
Scarlet fever
EBV

144
Q

What are some diagnostic tests to diagnose Erythema Infectiosum?

A

Most is made on clinical grounds – suspect it if biphasic illness and facial rash

Adults 25-50% are asymptomatic.

B19 specific IgM indicates current or recent infection

B19 specific IgG indicates immunity

PCR

145
Q

What are some complications of Erythema Infectiosum?

A

Parvovirus B19 suppresses erythropoiesis for about a week so can cause anaemia

Affects pregnant woman and is hard to distinguish between rubella.

146
Q

What is the management of Erythema Infectiosum in bairns and pregnant women?

A

Simple Analgesia – paracetamol/ibuprofen –> conservative treatment.

No longer infectious once the rash has developed

Make sure no contact with immunocompromised or pregnant women through prodrome.

Pregnant women

Can affect an unborn baby in the first 20 weeks of pregnancy –> woman should have maternal IgM and IgG checked.

147
Q

What is Henoch Schonlein Purpura?

A

HSP is an IgA mediated AI hypersensitivity vasculitis of childhood. It is usually seen in children following an infection –> Affects skin, joint, gut and kidneys

148
Q

What are some risk factors for HSP?

A
  • Infections (Group A strep, mycoplasma and EBV)
  • Vaccinations
  • Exposure to allergens, cold, pesticides
  • Insect bite
149
Q

What is the clinical presentation of HSP?

What rash is normal?

A

Palpable purpuric rash (with localised oedema) over buttocks and extensor surfaces of arms and legs

Fever
Abdo pain/symptoms
Renal involvement – features of IgA nephropathy – haematuria/renal failure.
Polyarthritis

150
Q

What is the prognosis of HSP?

A

Usually excellent, HSP is usually a self-limiting condition. 1/3 will relapse.

Relapses usually milder.

Prognosis better if no renal problems.

151
Q

What is the diagnostic tests involved in HSP?

A

Clinical features

Urinalysis – protein/haematuria  if kidney damage suspected

Raised ESR, Serum IgA, WCC

Anti-streptolysin O titrates increased (36%) – detect group A strep

152
Q

What is the management of HSP?

A

Analgesia for arthralgia - Paracetamol

Treatment of nephropathy is generally supportive.

Corticosteroids for severe symptoms like abdo pain/kidney damage

153
Q

What is Klinefelter’s syndrome?

A

Associated with karotype 47XXY - the chief genetic cause of hypogonadism

154
Q

What is the clinical presentation of Klinefelter’s syndrome?

A 
Gynaecomastia 
Infertility
Taller than average
Small testes/penis 
Delayed/absent puberty
Less body hair, broader hips, longer legs
155
Q

What are some things associated with Klinefelter’s syndrome?

A

psychosocial issues, learning disability, AI disease, osteoporosis, Decreased sexual maturation

Lifespan is normal - arm span may be longer than normal length.

156
Q

What is the management of Klinefelter’s syndrome?

A
  • Androgen therapy

- Mastectomy – gynaecomastia

157
Q

What is Impetigo?

A

Superficial bacterial skin infection

158
Q

What are the clinical features of impetigo?

A

Fever

Very contagious and Incubation period is 4-10 days

Well defined lesions starting around nose and face with honey/golden coloured crusts on erythematous base

159
Q

What are the causes of Impetigo?

A

Primary infection - Staph aureus or Strep pyogenes

Can also be a complication of an existing condition – eczema, scabies or insect bites.

160
Q

How can you diagnose Impetigo?

A

Usually clinical features

Can swab the exudate of a moist or deroofed blister for culture

161
Q

What is the appropriate management of Impetigo?

A

First line NICE – Hydrogen peroxide 1% cream for those not systematically unwell or at high risk of complications

If unsuitable abx - short course for 5 days.

Topical antibiotic creams – Topical Fusidic acid or mupirocin if resistance is suspected

Severe disease – oral flucloxacillin or erythromycin if penicillin allergic

162
Q

How long should a person be excluded from school with impetigo?

A

Children should be excluded from school until lesions are crusted and healed or 48 hrs after Abx treatment has started.

163
Q

What is Down Syndrome?

A

A genetic condition caused by Trisomy 21. It causes a large amount of systemic complications and has several characteristic facial features.

164
Q

What are two risk factors for Down Syndrome?

A

Family history

Older maternal age- >40 increases risk of non-disjunction

165
Q

What Facial Features are associated with Down Syndrome?

A
  • Epicanthic folds
  • Protruding tongue
  • Small low set ears
  • Flat occiput + facial profile
  • High arched palate
166
Q

What are some of the Complications associated with Down Syndrome?

Think

GI
Eyes
Cardio
Ears
Orthopaedic
Endocrine
Neuro
Haematological
A

Cardio – VSD/TOF (40/50%)

GI – Atresia’s, Hirschsprung’s, pyloric stenosis, Meckel’s diverticulum

Eyes – Brushfield spots, cataracts, nystagmus, strabismus

Ears – 90% have hearing loss – sensorineural and conducive

Orthopaedic – Hypotonia, short stature, single palmar crease, sandal gap deformity

Endocrine - hypothyroid

Neuro – Learning difficulties, low IQ, seizures, dementia (Alzheimer’s)

Haematological – 12x greater risk of infections due to impaired cellular immunity, increase risk of AML, ALL and polycythaemia

167
Q

Describe the testing for Down Syndrome at:

11-13 weeks

A

Antenatal testing – Combined test is now standard and is done between 11-13 weeks.

Nuchal Translucency measurement + serum B-HCG + pregnancy associated plasma protein A

Down’s is suggested by – Elevated B-HCG, decreased PAPP-A and thickened nuchal translucency

Trisomy 18 (Edwards) and 13 (Patau) give similar results but PAPP-A tends to be lower.

168
Q

Describe the testing for Down Syndrome at 15-20 weeks.

A

If women book later in pregnancy 15-20 weeks then they should be offered the triple/quadruple test

triple test: alpha-fetoprotein, unconjugated oestriol, human chorionic gonadotrophin

quadruple test: alpha-fetoprotein, unconjugated oestriol, human chorionic gonadotrophin and inhibin-A

169
Q

What is Childhood disability and what are two examples?

A

Physical or mental impairment preventing them going about their daily life

  • Downs
  • Cerebral palsy
170
Q

What are the postural reflexes?

A
  • Parachute
  • Positive support
  • Landau
  • Neck/head righting reflexes
  • Lateral propping
171
Q

What does a persistence of primitive reflexes and lack of postural reflexes indicate?

A

Hallmark of motor neuron abnormality in the infant.

172
Q

What are the primitive reflexes?

A

Primitive reflexes

A Tonic neck reflex

Moro reflex

Landau reflex

Plantar/palmar grasp reflex
Parachute reflex
Positive support reflex

Rooting reflex

Stepping reflex

Trunk incurvation

A M L PPPP R S T

173
Q

What is the Tonic Neck Flex?

How long does it last for?

A

Baby supine, turn head to one side and hold jaw on shoulder

Arms/legs the heads turned to will extend and the opposite will flex

Until 6 months

174
Q

What is the Moro Reflex?

How long does it last for?

A

Hold baby supine and abruptly lower the body about 2 feet

Arms will abduct/extend, and legs will flex

Lasts until 2 months

175
Q

What is the Landau reflex?

A

Suspend baby prone

Head will lift and the spine will straighten

lasts from 0-6 months

176
Q

What is the Plantar Reflex?

A

Touch hand/soles and baby will grasp/curl toes.

Until 9-12 months

177
Q

What is the parachute reflex?

A

Suspend baby prone and slowly lower the head towards a surface

Arms and legs will extend in a protective fashion

8 months onwards

178
Q

What is the positive support reflex?

A

Hold baby upright until feet touch the surface

Hips, knees, and ankles will extend and partially bear weight for 20/30 seconds

0-6 months

179
Q

What is the sucking and rooting reflex?

A

Stroke perioral skin at corner of the mouth

Mouth will open and baby will turn head towards stimulus and suck

Until 4 months

180
Q

What is the stepping reflex and when should it be seen?

A
  • Hold baby upright with one sole on table top
  • Hip and knee will flex and other footstep forward
  • Birth – variable (6weeks)
181
Q

What is Trunk Incurvation/galant reflex?

A

Support baby prone and stroke one side of the back

Spine will curve towards the stimulated side

Lasts 0-2 months.

182
Q

What is Patau Syndrome?

A

Severe physical and mental congenital abnormalities due to Trisomy 13

183
Q

What is the presentation of Patau Syndrome?

A

Key feature – microcephalic, small eyes, cleft lift/palate, and scalp lesions

  • Congenital heart defects
  • IUGR and low BW
  • Polydactyl and rocker bottom feet
  • Severe learning difficulties
  • Cleft lip palate

Holoprosencephaly – Brain doesn’t divide into two halves

184
Q

What are the facial features of Patau Syndrome?

A

Cleft lip and palate

Hypotelorism (reduced distance between the eyes)

Microphthalmia

185
Q

What is the prognosis of Patau Syndrome?

A
  • Prognosis is bad – average survival is 2.5 days
  • 50% live longer than one week
  • 5-10% live longer than one year
186
Q

What is Steven-Johnson Syndrome?

A

Severe systemic reaction affecting the skin and mucosa that is almost always caused by a drug reaction.

187
Q

What are some causative drugs of Steven-Johnsons Syndrome?

A

Sulphonamides

Allopurinol

Anti-epileptics – Lamotrigine, carbamazepine, phenytoin

Penicillin

NSAIDs

OCP

188
Q

What is the presentation of Steven-Johnson Syndrome?

A

Painful erythematous macules, severe mucosal ulceration

Early flu like symptoms – cough, red eyes, sore throat, tender pink skin

Fever

189
Q

What is the diagnosis of steven-johnson syndrome?

A

Symptoms + clinical history

Biopsy

190
Q

What is the appropriate management of Steven-Johnson syndrome?

A

Triggering medication stopped

Hospitalisation for treatment

Treat the infection

Antihistamines, IVIG or Corticosteroids for hypersensitivity response

Hydration, wound care and analgesia.

191
Q

What is Edwards syndrome?

A

Trisomy 18 – 80% are female – severe psychomotor + growth retardation in those that survive the 1st year of life.

192
Q

What are some risk factors for Edwards syndrome?

A
  • Advancing maternal age
  • Family history
  • Being female
193
Q

How can you diagnose Edwards syndrome?

A

Confirmed by karyotyping

Ultrasound for nuchal translucency

Prenatal sonogram – suggestive is shows polyhydramnios

Serum markers – first trimester – HCG and PAPP-A down

Serum markers – second – AFP and unconjugated estriol down

Inhibin A typically normal or down.

194
Q

What is the key features of Edwards Syndrome?

A

micrognathia, low set ears, rocker bottom feet, overlapping of fingers

195
Q

What are some skeletal abnormalities associated with Edwards syndrome?

A
  1. Typical hand feature
  2. Radial + thumb aplasia
  3. Short sternum – nipples look widely spread
  4. Rocker bottom feet -flat feet
  5. Microcephaly/microstomia
196
Q

What are some craniofacial abnormalities associated with Edwards Syndrome?

A
  • Odd low set ears
  • Micrognathia (small jaw)
  • Prominent occiput
197
Q

What is the typical hand posture in Edwards Syndrome?

A
  • Fingers cannot be extended
  • Index overrides middle finger
  • 5th finger overriding the 4th finger
198
Q

What are some further complications that someone with Edwards Syndrome may suffer from?

Think;

GI 
Cardiac
Risk of developing tumours
Infection
Pulmonary
A

GI issues – oesophageal Atresia and omphalocele
Congenital heart defects – Septal defects & PDA
Risk of developing wilms tumour (nephroblastoma)
Frequent infections
Breathing problems due to pulmonary hypoplasia

199
Q

What is Neurofibromatosis?

A

Neurofibromatosis – AD disorder that encompasses NF1, NF2 and Schwannomatosis

200
Q

What is NF1, NF2 and Schwannomatosis?

A

NF1 – More common and caused by a defect to the NF1 gene-skin lesions

NF2 – Central form with CNS tumours rather than skin lesions
- Inherited schwannomas, typically bilaterally, also meningiomas and ependymomas

Schwannomatosis – Recently recognised form, characterised by multiple non cutaneous schwannomas which is a histologically benign nerve sheath tumour

201
Q

What is the cause of NF1?

A

Gene mutation on chromosome 17 which encodes neurofibromin

Affects 1 in 4000.

202
Q

What is the diagnostic criteria of NF1?

A

2 or more of:

6+ café-au-lait spots (>5mm in kids and >15mm in adults)

2 or more neurofibromas

Freckling of skin folds

Optic glioma

Lisch nodules (clumps of pigment in the eyes)

Boney abnormalities (sphenoid dysplasia – absence of bone around eyes)

Parent or sibling with NF1

203
Q

What is the clinical presentation of NF1?

A
  • Café-au-lait spots
  • Freckling in skin folds
  • Neurofibromas
  • Lisch nodules
  • Short stature and macrocephaly
204
Q

What are some complications of Neurofibromatosis?

A
  • Mild learning difficulties
  • Nerve root compression from neurofibromas
  • Increased risk of malignancies e.g. optic glioma
205
Q

What is the treatment of Neurofibromatosis?

A

Intervene appropriate where tumours produce pressure symptoms or indicate malignant change - Possible surgery

Physiotherapy

Psychotherapy

206
Q

What is the cause of Neurofibromatosis type 2?

A

Gene mutation on chromosome 22 and affects 1 in 100,000

207
Q

What is the presentation of Neurofibromatosis Type 2?

A

45% have hearing issues

Schwannomas bilaterally, especially vestibular nerve (cranial/spinal)

Meningiomas/ependymomas

Presents generally in 20s

208
Q

What investigations can be used to diagnose Neurofibromatosis?

A
  • Examination + symptoms
  • Biopsy
  • MRI, x-ray and CT scans
  • Blood tests – genetic testing
209
Q

What is Otitis Media?

A

Infection of the middle ear due to short, horizontal eustachian tubes and mucal discharge almost always from the middle ear.

210
Q

What is the pathophysiology of Otitis Media?

A

Viral URTIs precede Otitis Media but most infections are secondary to bacterial infection:

Strep Pneumonaie, Haemophilus Influenzae and Moraxella catarrhalis

Viral URTIs are thought to disturb the nasopharyngeal microbiome, introducing bacteria.

211
Q

What is the epidemiology of Otitis Media?

A

Incredibly common in children with around half of children having 3 or more episodes by year 3.

212
Q

What are the symptoms of Otitis Media?

A
  • Rapid onset ear pain – bulging of the tympanic membrane
  • Pyrexia – 50%
  • Recent viral URTI symptoms are common
  • Otorrhoea – discharge from the ear
213
Q

What is the biggest cause of hearing loss in bairns?

A

Otitis media with effusion or glue ear

214
Q

What is some of the criteria to diagnose Otitis Media?

A

Acute onset of symptoms – otalgia or ear tugging

Presence of middle ear infection – bulging of tympanic

Inflammation of the tympanic membrane

215
Q

What are some possible otoscopy findings in Otitis Media?

A

Bulging tympanic membrane – loss of light reflex

Opacification of erythema of the tympanic membrane

Perforation with purulent otorrhea

Decreased mobility if using a pneumatic otoscope

216
Q

What is the usual management of Otitis Media?

A

Usually self limiting

Give analgesia

If criteria met - 5-7 day course of amoxicillin or if allergic - erythromycin or clarithromycin.

217
Q

What is the criteria for giving antibiotics in Otitis Media?

A

Symptoms lasting more than 4 days or not improving

Systemically unwell but not requiring admission

Immunocompromise or high risk complications secondary to heart, lung, kidney, liver, NM disease

Younger than 2 years old with bilateral otitis media

Otitis media with perforation/discharge in canal.

218
Q

What is Toxic Shock Syndrome?

A

A severe systemic reaction to staphylococcal exotoxins which acts as a super antigen and can cause organ dysfunction can be released from any infection site.

219
Q

What can cause Toxic shock syndrome?

A

Staph exotoxins e.g. Staph Aureus

220
Q

What is the presentation of Toxic Shock Syndrome?

A
  • Dizziness, fainting, Breathing problems
  • Flu like symptoms – headache, feeling cold, fatigued, aching body, sore throat
  • Fever >39 degrees
  • Hypotensive
  • Diffuse erythematous, macular rash

Involvement of three or more organ systems e.g. Gastroenteritis, mucous membrane erythema, renal failure, hepatitis, thrombocytopenia, CNS involvement (confusion).

221
Q

What is the management of Toxic Shock Syndrome?

A
  • Intensive care if severe
  • Removal of infection focus e.g. tampon
  • IV fluids
  • ABX – ceftriaxone + clindamycin
222
Q

What is Autism?

A

Neurodevelopmental disorder that includes a range of possible impairments in social interaction, repetitive behaviour, and communication.

The presence of abnormal or impaired development that is manifest before the age of 3

223
Q

What is the Epidemiology of Autism?

A

Prevalence 1-2%, ASD is seen 3-4x as much in boys and around 50% have an intellectual disability

224
Q

What are 3 characteristics of abnormal functioning in autism?

A
  • Reciprocal social interaction
  • Impairment of language and communication
  • Restricted repetitive behaviour
225
Q

What are some signs of abnormal functioning in autism?

A
  • Communication problems
  • Social interaction issues
  • Social imagination issues
  • Sensory issues
226
Q

What are some social interaction issues some children may display?

A

Overly friendly/shy

Struggles to understand social roles

Often no desire to interact with others

Touches inappropriately, plays alone, poor eye contact, finds it hard to take turns

227
Q

What are some social imagination issues children may display?

A
  • Struggles with change
  • Obsessions/rituals
  • Repetitive with play
  • Unable to play or write imaginatively
228
Q

What are some communication difficulties that a child with autism might display?

A

Repeats speech

Disordered language

Poor non-verbal communication

No social awareness, unable to start up or keep a convo

229
Q

What are some associated conditions with autism?

A
  • Epilepsy around 20%
  • Visual and hearing impairment
  • Mental health (ADHD, depression and anxiety)
230
Q

What are some treatments for autism?

A

Education and games to encourage social communication

Visual aids and timetables

Parenting workshops and school liaison as well as family support & counselling

231
Q

What is the pharmacological management of Autism?

A

Methylphenidate – ADHD

Antipsychotic drugs e.g. risperidone – useful to treat self-injury, aggression

SSRIs – reduce repetitive stereotyped behaviour, anxiety and aggression.

Melatonin for sleep difficulties

232
Q

What is Asperger’s Syndrome?

A

Pervasive development disorder which lies within the autistic spectrum

Boys 8:1 girls

233
Q

How is Asperger’s different to autism?

A

Lack of delayed cognition and language

Above average intelligence

More likely to seek social interaction and share activities/friendships

234
Q

What is the clinical presentation of Aspergers?

A
  • Obsessed with complex subjects
  • Concrete thinking
  • Pedantic
  • Normal speech
  • Clumsiness
  • Solitary but socially aware
  • Poor sleep patterns

Phase 3a Medicine Sheffield (2 decks)

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