ILOs 1 Flashcards

1
Q

Give some causes of global developmental delay

A

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

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2
Q

Give some causes of gross motor delay

A

Cerebral palsy
Ataxia
Myopathy
Spina bifida
Visual impairment

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3
Q

Give some causes of fine motor delay

A

Dyspraxia
Cerebral palsy
Muscular dystrophy
Visual impairment

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4
Q

Give some causes of speech and language delay

A

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

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5
Q

Give some causes of social delay

A

Emotional and social neglect
Parenting issues
Autism

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6
Q

What are the main types of pneumothorax seen in children?

A

spontaneous pneumothorax:

  1. primary spontaneous pneumothorax (PSP): Occurs without underlying lung disease, often in tall, thin, young individuals, associated with the rupture of subpleural blebs or bullae
  2. secondary spontaneous pneumothorax (SSP): Occurs in patients with pre-existing lung disease, such as asthma, CF and pneumonia. Certain connective tissue diseases such as Marfan’s syndrome are also a risk factor

traumatic pneumothorax

iatrogenic pneumothorax

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7
Q

What are the sxs and signs of a simple pneumothorax?

A

Symptoms tend to come on suddenly:
dyspnoea
pleuritic chest pain

Signs
hyper-resonant lung percussion
reduced breath sounds
reduced lung expansion
tachypnoea
tachycardia

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8
Q

What is a tension pneumothorax?

A

a severe pneumothorax

occurs when a one way valve is created between the lung and the pleura, which leads to an accumulation of air within the pleural cavity = increase in intrathoracic pressure

results in the displacement of mediastinal structures that may result in severe respiratory distress and haemodynamic collapse

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9
Q

What are the signs of tension pneumothorax?

A

tracheal deviation away from the side of the pneumothorax
hypotension, tachycardia, tachypnoea
quiet heart sounds
cyanosis

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10
Q

Management in primary pneumothorax without shortness of breath, and <2cm in size?

A

discharge and review

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11
Q

Management of pneumothorax with a rim of air >2cm or clinically short of breath (SOB)?

A

Chest drain insertion

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12
Q

What is the safe triangle for chest drain insertion?

A

The triangle is located in the mid axillary line of the 5th intercostal space.

It is bordered by:
Anterior edge latissimus dorsi, the lateral border of pectoralis major, a line superior to the horizontal level of the nipple, and the apex below the axilla.

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13
Q

How can you find out a chest drain is in the right place without doing a CXR?

A

Chest drain swinging: water level rises on inspiration, falls on expiration

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14
Q

How should a suspected tension pneumothorax be investigated and managed?

A

A tension pneumothorax should not be investigated if suspected but should be immediately decompressed with a needle (14G needle, 2nd intercostal space)

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15
Q

How can poisoning of unknown origin be investigated?

A

can consult NPIS or TOXBASE for advice

Blood tests, such as toxicological investigations, FBC, U&Es, LFTs, glucose, clotting and arterial blood gases

urine drug screen

ECG

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16
Q

How can poisoning of unknown origin be managed?

A

can consult NPIS or TOXBASE for advice

Activated charcoal can bind to the poison and prevent absorption - up to 1 hour after ingestion

Alkalinisation of the urine for salicylate poisoning

Haemodialysis for ethylene glycol, lithium, methanol, phenobarbital, salicylates, and sodium valproate

Antidotes (if available) may be given for certain poisons

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17
Q

Give some key clinical features of malnutrition in children

A

High susceptibility to infections
Slow or poor wound healing
bradycardia, hypotension, and hypothermia
Depleted subcutaneous fat stores
Low skeletal muscle mass

In children, other indicators of undernutrition include:
Wasting: low weight for height
Stunting: low height for age
Underweight: low weight for age

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18
Q

Give some complications of malnutrition

A

Impaired immunity (increased risk of infections)
Poor wound healing
Growth restriction in children
Unintentional weight loss, specifically the loss of muscle mass
Multi-organ failure
Death

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19
Q

What signs should you look for on examination of a malnourished child?

A

shock: lethargic or unconscious; with cold hands, slow capillary refill (> 3 s), or weak (low volume), rapid pulse and low blood pressure
signs of dehydration e.g. decreased skin turgor
severe palmar pallor
bilateral pitting oedema
eye signs of vitamin A deficiency

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20
Q

What is Marasmus?

A

overt loss of adipose tissue and muscle as a result of total calorie insufficiency

children appear emaciated, weak and lethargic, and have associated bradycardia, hypotension, and hypothermia

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21
Q

What is Kwashiorkor?

A

‘the sickness of the weaning’ - often occurs on cessation of breastfeeding
severe protein deficiency with fair caloric intake
hypoalbuminaemia may cause bilateral pitting oedema and distended abdomen due to ascites

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22
Q

How should you assess a malnourished child?

A

detailed dietary history and physical examination

anthropometric measurements (including weight, length, and head circumference in younger children)

skinfold thickness and mid-upper-arm circumference (MUAC)

U&Es, LFTs, serum albumin levels

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23
Q

How should you manage a malnourished child?

A

treat hypoglycaemia
treat / prevent any hypothermia
rehydrate
refeed slowly with regular refeeding bloods

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24
Q

How should you dx and tx hypoglycaemia in a child?

A

take capillary BM - blood glucose below < 3 mmol/litre = hypoglycaemia

Give 50 ml of 10% glucose solution orally or by nasogastric tube
If the child is unconscious, treat with IV 10% glucose at 5 ml/kg

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25
How can you dx and mx hypothermia in a child?
If the axillary temperature is < 35 °C or does not register on a normal thermometer, assume hypothermia. When a low-reading thermometer is available, rectal temperature (< 35.5 °C) confirms hypothermia Re-warm the child: Make sure the child is clothed (especially the head); cover with a warmed blanket and place a heater or lamp nearby, or put the child on the mother's bare chest or abdomen (skin-to-skin) treat for potential hypoglycaemia and infection Feed immediately and again every 2 hours
26
What atrial septal defects may be seen in children?
Ostium secondum : septum secondum fails to fully close, leaving a hole in the wall Patent foramen ovale: foramen ovale fails to close (although this not strictly classified as an ASD) Ostium primum: septum primum fails to fully close, leaving a hole in the wall. This tends to lead to atrioventricular valve defects
27
What are the potential complications of ASDs in children?
Stroke in the context of venous thromboembolism Atrial fibrillation or atrial flutter Pulmonary hypertension and right sided heart failure Eisenmenger syndrome - reversal of left to right shunt due to pulmonary hypertension
28
What may be heard on auscultation of an ASD?
mid-systolic, crescendo-decrescendo murmur loudest at the upper left sternal border with a fixed split second heart sound (doesn't change with inspiration or expiration)
29
How may ASDs present in children?
may be picked up on antenatal screening / newborn examination may be symptomatic: Shortness of breath Difficulty feeding Poor weight gain Lower respiratory tract infections may be asymptomatic in childhood and present in adulthood with dyspnoea, heart failure or stroke
30
How can ASDs be managed?
should be referred to a paediatric cardiologist for ongoing management If the ASD is small and asymptomatic, watching and waiting can be appropriate can be corrected surgically using a transvenous catheter closure (via the femoral vein) or open heart surgery anticoagulants (such as aspirin, warfarin and NOACs) are used to reduce the risk of clots and stroke
31
What conditions are commonly associated with VSDs in children?
Down’s Syndrome and Turner’s Syndrome
32
What is the usual direction of flow of blood in a VSD? What may this cause?
from left to right patient remains acyanotic but too much blood flow into the lungs may cause right sided overload / right heart failure pulmonary hypertension may cause reversal of the shunt (Einsenmengers syndrome)
33
What sxs may VSDs present with?
Poor feeding Dyspnoea Tachypnoea Failure to thrive
34
What may be heard on auscultation of the chest of a patient with a VSD?
pan-systolic murmur more prominently heard at the left lower sternal border in the third and fourth intercostal spaces may be a systolic thrill on palpation
35
How should VSDs be managed?
referred to paediatric cardiologist small VSDs with no symptoms or evidence of pulmonary hypertension / HF can be watched and often close spontaneously can be corrected surgically using a transvenous catheter closure via the femoral vein or open heart surgery increased risk of infective endocarditis in patients with a VSD =antibiotic prophylaxis should be considered during surgical procedures
36
Give some symptoms of aortic stenosis
fatigue, shortness of breath, dizziness and fainting sxs typically worse on exertion as the outflow from the left ventricle cannot keep up with demand severe aortic stenosis will present with heart failure within months of birth.
37
Describe the murmur heard in aortic stenosis
ejection systolic murmur heard loudest at the aortic area (second intercostal space, right sternal border) It has a crescendo-decrescendo character and radiates to the carotids
38
Besides a murmur, what might you find on examination of aortic stenosis?
Ejection click just before the murmur Palpable thrill during systole Slow rising pulse and narrow pulse pressure
39
How can aortic stenosis be investigated and managed?
gold standard for dx is an echocardiogram monitoring with regular echos, exercise testing and ECGs Mx options: Percutaneous balloon aortic valvoplasty Surgical aortic valvotomy Valve replacement
40
Give some complications of aortic stenosis
Left ventricular outflow tract obstruction Heart failure Ventricular arrhythmia Bacterial endocarditis Sudden death, often on exertion
41
What conditions may be associated with congenital pulmonary valve stenosis?
Tetralogy of Fallot William syndrome Noonan syndrome Congenital rubella syndrome
42
Give some signs of pulmonary stenosis found on examination
Ejection systolic murmur heard loudest at the pulmonary area (second intercostal space, left sternal border) Palpable thrill in the pulmonary area Right ventricular heave due to right ventricular hypertrophy Raised JVP with giant a waves
43
How should pulmonary stenosis be investigated and managed?
ix = echo mild = watch and wait symptomatic = balloon valvuloplasty via a venous catheter (femoral vein > IVC > right side of the heart > pulmonary valve)
44
Allergic rhinitis is a condition caused by an IgE-mediated type 1 hypersensitivity reaction, where environmental allergens cause an allergic inflammatory response in the nasal mucosa. How can it be classified?
Seasonal, for example hay fever Perennial (year round), for example house dust mite allergy Occupational, associated with the school or work environment
45
Presentation of allergic rhinitis?
Runny, blocked and itchy nose Sneezing Itchy, red and swollen eyes personal / family hx of atopy
46
How can allergic rhinitis be managed?
Avoid the trigger : hoovering, changing pillows regularly and good ventilation of the home for dust mite allergy; staying indoors during high pollen counts for hay fever; minimising contact with pets that trigger Non-sedating antihistamines e.g. cetirizine, loratadine and fexofenadine Nasal corticosteroid sprays such as fluticasone and mometasone Referral to paediatric allergy specialist if unmanageable
47
Good technique for using nasal spray?
Hold the spray in the left hand when spraying into the right nostril and vice versa. Aim to spray slightly outward, away from the nasal septum. Do NOT sniff at the same time as spraying, as this sends the mist straight to the back of the throat.
48
What is urticaria? How can it be managed?
local or generalised superficial swelling of the skin pale, pink raised skin, also called 'hives' or 'wheals' pruritic mx: non-sedating antihistamines are first-line prednisolone is used for severe or resistant episodes
49
Give some causes of acute urticaria
Allergies to food, medications or animals Contact with chemicals, latex or stinging nettles Medications Viral infections Insect bites Dermatographism (rubbing of the skin)
50
Give some causes of AKI
prerenal: hypovolaemia secondary to diarrhoea/vomiting, sepsis renal: glomerulonephritis acute tubular necrosis (ATN) acute interstitial nephritis (AIN) rhabdomyolysis post-renal: kidney stone in ureter or bladder
51
Give some sxs and signs of AKI
reduced urine output pulmonary and peripheral oedema arrhythmias (deranged electrolytes) features of uraemia (e.g. pericarditis or encephalopathy)
52
What causes ARPCKD?
mutation in the polycystic kidney and hepatic disease 1 (PKHD1) gene on chromosome 6
53
How does ARPCKD present?
oligohydramnios and polycystic kidneys seen on antenatal scans lack of amniotic fluid can lead to Potter syndrome: dysmorphic features such as low set ears, a flat nasal bridge, skeletal abnormalities, pulmonary hypoplasia, and respiratory failure shortly after birth
54
What complications may children with ARPCKD face in later life?
Liver failure and portal htn due to liver fibrosis Progressive renal failure Hypertension due to renal failure Chronic lung disease
55
What is Multicystic dysplastic kidney (MCDK)?
where one of the baby’s kidneys is made up of many cysts while the other kidney is normal, normally diagnosed on antenatal ultrasound scans often the cystic kidney will atrophy and disappear before 5 years of age having a single kidney can put the person at risk of UTI, hypertension and CKD
56
What is nephritis?
inflammation within the nephrons of the kidneys. It causes: Reduction in kidney function Haematuria Proteinuria
57
What are the two most common causes of nephritis in children?
post-streptococcal glomerulonephritis and IgA nephropathy (Berger’s disease)
58
How does post-streptococcal glomerulonephritis present? Mx?
occurs 1 – 3 weeks after a β-haemolytic streptococcus infection, such as tonsillitis caused by Streptococcus pyogenes may be hx of tonsillitis, positive throat swab results or anti-streptolysin antibody titres found on blood test supportive mx, may use antihypertensive medications and diuretics for complications
59
What will you see on histological examination of renal biopsy for Berger's disease?
IgA deposits and glomerular mesangial proliferation
60
Outline the presentation and mx of IgA nephropathy (Berger's disease)?
Frank haematuria following upper resp tract infection in young person related to Henoch-Schonlein Purpura, which is an IgA vasculitis Mx: supportive treatment of the renal failure and immunosuppressant medications such as steroids and cyclophosphamide to slow the progression
61
What is Haemolytic uraemic syndrome (HUS)?
thrombosis in small blood vessels throughout the body, usually triggered by Shiga toxins from either E. coli or Shigella classic triad of: Microangiopathic haemolytic anaemia Acute kidney injury Thrombocytopenia (low platelets)
62
How does HUS present?
Diarrhoea is the first symptom, which turns bloody within 3 days. Around a week after the onset of diarrhoea, the features of HUS develop: Fever Abdominal pain Haematuria Hypertension Bruising Jaundice (due to haemolysis) Confusion, lethargy
63
How does HUS present on investigation?
FBC (thrombocytopenia), U&Es (deranged), creatinine peripheral blood smear = broken red cells blood culture to rule out septicaemia
64
How should HUS be managed?
hospital admission and supportive management with treatment of: Hypovolaemia (e.g., IV fluids) Hypertension Severe anaemia (e.g., blood transfusions) Severe renal failure (e.g., haemodialysis)
65
How does oral candidiasis present in children?
white or creamy patches on the tongue, inner cheeks, gums, tonsils, or roof of the mouth. These patches may be painful or cause discomfort while eating or drinking = reduced feeding / avoidance behaviours
66
How can oral candidiasis in kids be managed?
Topical antifungals are considered first-line therapy for mild-to-moderate cases of oral candidiasis: Nystatin suspension Miconazole gel
67
Cellulitis is a bacterial infection of the dermis and subcut tissues most commonly caused by infection with Streptococcus pyogenes. How does it present?
commonly occurs on the shins, usually unilateral erythema (generally well-defined margins but some cases may present with diffuse erythema) blisters and bullae may be seen swelling systemic upset: fever, malaise, nausea
68
How is cellulitis diagnosed and managed?
clinical dx - no ix required oral flucloxacillin as first-line treatment for mild/moderate cellulitis oral clarithromycin or doxycycline if penicillin allergic
69
Conjunctivitis is the most common eye problem presenting to primary care. It is characterised by sore, red eyes associated with a sticky discharge. How does it present differently if bacterial or viral?
Bacterial conjunctivitis Purulent discharge Eyes may be 'stuck together' in the morning Viral conjunctivitis Serous discharge Recent URTI Preauricular lymph nodes
70
How can infective conjunctivitis be managed?
normally a self-limiting condition that usually settles without treatment within 1-2 weeks topical antibiotic therapy e.g. Chloramphenicol drops (given every 2-3 hourly initially) advice should be given not to share towels school exclusion is not necessary
71
How can herpes simplex infection present?
primary infection: may present with a severe gingivostomatitis cold sores painful genital ulceration
72
How can herpes simplex infection be managed?
gingivostomatitis: oral aciclovir, chlorhexidine mouthwash cold sores: topical aciclovir genital herpes: oral aciclovir
73
Falciparum malaria is the commonest, and most severe, type of malaria. Describe the key presenting features
Feature of severe malaria: hypoglycaemia acidosis temperature > 39 °C severe anaemia schizonts on a blood film parasitaemia > 2%
74
What are the major complications of severe falciparum malaria?
hypoglycaemia cerebral malaria: seizures, coma acute renal failure acute respiratory distress syndrome (ARDS) DIC shock may indicate coexistent bacterial septicaemia - malaria rarely causes haemodynamic collapse
75
First line tx for uncomplicated falciparum malaria?
WHO guidelines recommend artemisinin-based combination therapies (ACTs) as first-line therapy examples include artemether plus lumefantrine, artesunate plus amodiaquine, artesunate plus mefloquine
76
First line tx for complicated falciparum malaria?
a parasite counts of more than 2% will usually need parenteral treatment irrespective of clinical state - IV artesunate or IV quinine dihydrochloride if parasite count > 10% then exchange transfusion should be considered
77
What is the most common cause of non-falciparum malaria?
Plasmodium vivax
78
How does non-falciparum malaria present?
general features of malaria: fever, headache, myalgia, anaemia, hepatosplenomegaly, jaundice Plasmodium vivax/ovale: cyclical fever every 48 hours, hypnozoite stage so may relapse following treatment. Plasmodium malariae: cyclical fever every 72 hours, associated with nephrotic syndrome.
79
How should non-falciparum malaria be treated?
in areas which are known to be chloroquine-sensitive then WHO recommend either chloroquine in areas which are known to be chloroquine-resistant an ACT should be used patients with ovale or vivax malaria should be given primaquine following acute treatment with chloroquine to destroy liver hypnozoites and prevent relapse
80
How is a diagnosis of malaria made?
malaria blood film - sent in an EDTA bottle (red) Need 3 samples over 3 consective days to exclude malaria due to 48 hour lifecyle can also do: FBC, U&Es, LFTs, glucose, coagulation CT head
81
What bacteria commonly cause acute otitis media?
Streptococcus pneumonaie, Haemophilus influenzae and Moraxella catarrhalis
82
How may otitis media present?
otalgia - children may tug or rub their ear fever, coryza hearing loss ear discharge may occur if the tympanic membrane perforates
83
Findings on otoscopy for otitis media?
bulging tympanic membrane → loss of light reflex opacification or erythema of the tympanic membrane perforation with purulent otorrhoea
84
How should otitis media be managed?
generally a self-limiting condition that does not require an antibiotic prescription, only analgesia abx if: Symptoms lasting more than 4 days Systemically unwell Younger than 2 years with bilateral otitis media Perforation and/or discharge in the canal 5-7 day course of amoxicillin is first-line
85
Complications of otitis media?
mastoiditis meningitis brain abscess facial nerve paralysis
86
Orbital cellulitis is the result of an infection affecting the fat and muscles posterior to the orbital septum, within the orbit. What are the risk factors?
Childhood (mean age of hospitalisation 7-12 yrs) Lack of Hib vaccination Previous sinus infection Recent eyelid infection/ insect bite on eyelid (periorbital cellulitis) Ear or facial infection
87
How may orbital cellulitis present?
Redness and swelling around the eye Eyelid oedema and ptosis Proptosis Severe ocular pain Ophthalmoplegia/pain with eye movements Visual disturbance
88
How can you differentiate between orbital and peri-orbital (pre-septal) cellulitis?
reduced visual acuity, proptosis, ophthalmoplegia/pain with eye movements are NOT consistent with preseptal cellulitis
89
How should orbital cellulitis be investigated?
Complete ophthalmological assessment – Decreased vision, afferent pupillary defect, proptosis, dysmotility, oedema, erythema FBC– WBC elevated, raised inflammatory markers Blood culture and swab (most common bacterial causes – Streptococcus, Staph aureus, HiB) CT with contrast – Inflammation of the orbital tissues deep to the septum, sinusitis
90
How should orbital cellulitis be managed?
admission to hospital for IV antibiotics
91
What ix can be done for children with recurrent infections?
FBC Immunoglobulins: B cell disorders Complement proteins: complement disorders Antibody responses to vaccines, specifically pneumococcal and haemophilus vaccines HIV test Chest x-ray for scarring from previous chest infections Sweat test for CF CT chest for bronchiectasis
92
Severe combined immunodeficiency (SCID) is the most severe condition causing immunodeficiency, with absent or dysfunctioning T and B cells. How does it present?
Persistent severe diarrhoea Failure to thrive Opportunistic infections e.g. severe and later fatal chickenpox, PJP and cytomegalovirus Unwell after live vaccinations such as the BCG, MMR and nasal flu vaccine Omenn syndrome
93
What is the genetic cause of most cases of SCID?
mutation in common gamma chain on the X chromosome that codes for interleukin receptors on T and B cells X-linked recessive inheritance
94
What is Omenn syndrome?
rare cause of SCID, autosomal recessive inheritance abnormally functioning and deregulated T cells that attack the tissues in the fetus erythroderma alopecia Diarrhoea, failure to thrive lymphadenopathy hepatosplenomegaly
95
How can SCID be managed?
treating underlying infections immunoglobulin therapy sterile environment avoiding live vaccines haematopoietic stem cell transplantation
96
What is Selective Immunoglobulin A Deficiency?
most common immunoglobulin deficiency patients have low levels of IgA and normal levels of IgG and IgM tendency to recurrent mucous membrane infections, such as LRTIs
97
What is Common variable immunodeficiency?
genetic mutation in the genes coding for components of B cells = deficiency in IgG and IgA recurrent respiratory tract infections unable to develop immunity to infections or vaccinations prone to immune disorders such as RA and cancers such as non-Hodgkins lymphoma
98
What is X-linked agammaglobulinaemia?
X-linked recessive condition results in abnormal B cell development and deficiency in all classes of immunoglobulins
99
What is DiGeorge syndrome?
22q11.2 deletion syndrome An underdeveloped thymus gland = inability to create functional T cells C – Congenital heart disease A – Abnormal facies (characteristic facial appearance) T – Thymus gland incompletely developed C – Cleft palate H – Hypoparathyroidism and resulting Hypocalcaemia 22nd chromosome affected
100
Important mx step in patients with complement deficiencies?
Vaccination against encapsulated organisms
101
Rubella, also known as German measles, is a viral infection caused by the togavirus. What features does it present with?
prodrome, e.g. low-grade fever rash: maculopapular, initially on the face before spreading to the whole body, usually fades by the 3-5 day lymphadenopathy: suboccipital and postauricular
102
Complications of rubella?
arthritis encephalitis myocarditis thrombocytopaenia
103
What is the FEVER PAIN criteria for diagnosis of tonsilitis?
Fever over 38°C Purulence (pharyngeal/tonsillar exudate). Attend rapidly (3 days or less) severely Inflamed tonsils No cough or coryza 0-1 = no abx 2-3 = consider abx 4-5 = abx almost definitely indicated
104
What abx are given if indicated in tonsillitis ?
if antibiotics are indicated then either phenoxymethylpenicillin or erythromycin (if the patient is penicillin allergic) should be given 7 or 10 day course should be given
105
Potential complications of tonsillitis?
Peritonsillar abscess or neck abscess Acute otitis media Acute sinusitis Acute post-streptococcal glomerulonephritis Streptococcal toxic shock syndrome Scarlet fever Acute rheumatic fever
106
How does staphylococcal toxic shock syndrome present?
fever hypotension diffuse erythematous rash desquamation of rash, especially of the palms and soles involvement of three or more organ systems: e.g. gastrointestinal (diarrhoea and vomiting), mucous membrane erythema, renal failure, hepatitis, thrombocytopenia, CNS involvement (e.g. confusion)
107
How is staphylococcal toxic shock syndrome managed?
removal of infection focus (e.g. retained tampon) IV fluids IV antibiotics