Paeds Derm + Infectious Disease + Allergy Flashcards
1
Q
How is sepsis risk calculated
A
quick SOFA score
2
Q
what is quick SOFA score
A
≥ 22 breaths/min RR
<15 GCS
≤ 100 mm Hg. sys
also coagulation (platelets) liver (bilirubin) and renal (creatine)
score of >2/3 = risk
3
Q
What is the traffic light system for assessment of children under 5 with fever in children
A
green (low risk), amber (intermediate risk) or red (high risk)
- color -> normal v. cyanosis
- activity –> alert v. absent & appears ill
- respiratory -> >40-50 RR v. red = >60 RR/ grunting
- circulation and hydration -> normal skin and moist membranes v. tachycardia dry membranes and poor skin turgor, cap refil >3sec
- other -> fever >5 days under 3 months, non blanching rash, seizures
4
Q
What is action for low risk in assessment of children under 5 with fever in children
A
Child can be managed at home with appropriate care advice, including when to seek further help
5
Q
What is action for moderate risk in assessment of children under 5 with fever in children
A
- F2F assessment to judge admission or not
- provide parents with a safety net or refer to a paediatric specialist for further assessment
6
Q
What is action for severe risk in assessment of children under 5 with fever in children
A
urgent admission
7
Q
What are signs of sepsis
A
- Deranged physical observations
- Prolonged capillary refill time (CRT)
- Fever or hypothermia
- Deranged behaviour
- Poor feeding
- Inconsolable or high pitched crying
- High pitched or weak cry
- Reduced consciousness
- Reduced body tone (floppy)
- Skin colour changes (cyanosis, mottled pale or ashen)
8
Q
What is the immediate management for sepsis
A
- Give oxygen if the patient has evidence of shock or oxygen saturations are below 94%
- Obtain IV access (cannulation)
- Blood tests, including a FBC, U&E, CRP, clotting screen (INR), blood gas for lactate and acidosis
- Blood cultures, ideally before giving antibiotics
- Urine dipstick and laboratory testing for culture and sensitivities
- Antibiotics according to local guidelines. They should be given within 1 hour of presentation.
- IV fluids. 20ml/kg IV bolus of normal saline if the lactate is above 2 mmol/L or there is shock. This may be repeated.
9
Q
What investigations can be ordered for sepsis
A
- Chest xray if pneumonia is suspected
- Abdominal and pelvic ultrasound if intra-abdominal infection is suspected
- Lumbar puncture if meningitis is suspected
- Meningococcal PCR blood test if meningococcal disease is suspected
- Serum cortisol if adrenal crisis is suspected
10
Q
What is septic shock
A
when sepsis has lead to cardiovascular dysfunction.
The arterial blood pressure falls, resulting in organ hypo-perfusion.
This leads to a rise in blood lactate as the organs begin anaerobic respiration.
11
Q
What is management if IV fluid boluses fail to improve the blood pressure and lactate level in children w septic shock
A
escalated to ICU + give inotropes (noradrenalin) to stimulate the cardiovascular system and improve blood pressure and tissue perfusion.
12
Q
What is Kawasaki’s
A
Medium vessel vasculitis
6m - 5yr M, AfroCarbb/Asian
13
Q
How does Kawasaki’s present
A
- persistent high fever (above 39ºC) for more than 5 days.
- strawberry tongue
- widespread erythematous maculopapular rash and desquamation on feet and hands
- conjunctivitis
- cervical lymphadenopathy
14
Q
How is Kawasaki’s investigated
A
FBC -> anaemia, leukocytosis and thrombocytosis
LFT -> hypoalbuminemia and elevated liver enzymes
Inflammatory markers -> ^ESR
Urinalysis -> ^WCC
Echocardiogram
15
Q
What is the disease course of Kawasaki’s
A
Acute Phase
Subacute Phase
Convalescent stage
16
Q
What is the Acute Phase of Kawasaki’s
A
The child is most unwell with the fever, rash and lymphadenopathy. This lasts 1 – 2 weeks.
17
Q
What is the Subacute Phase of Kawasaki’s
A
The acute symptoms settle, the desquamation and arthralgia occur and there is a risk of coronary artery aneurysms forming. This lasts 2 – 4 weeks.
18
Q
What is the Convalescent Phase of Kawasaki’s
A
remaining symptoms settle, the blood tests slowly return to normal and the coronary aneurysms may regress. This last 2 – 4 weeks.
19
Q
How is Kawasaki’s managed
A
- High dose aspirin to reduce the risk of thrombosis
- IV immunoglobulins to reduce the risk of coronary artery aneurysms
- Echo
20
Q
what is a complication of Kawasaki’s
A
coronary artery aneurysms
21
Q
Why is aspirin usually avoided in children
A
risk of Reye’s syndrome.
22
Q
What is Inactivated vaccines
A
giving a killed version of the pathogen
cannot cause an infection
are safe for immunocompromised patients
23
Q
give an example of Inactivated vaccines
A
Polio - salk version
Flu vaccine
Hepatitis A
Rabies
24
Q
what is Subunit and conjugate vaccines
A
only contain parts of the organism used to stimulate an immune response
cannot cause infection
are safe for immunocompromised patients.
25
give an example of Subunit and conjugate vaccines
Pneumococcus
Meningococcus
Hepatitis B
Pertussis (whooping cough)
Haemophilus influenza type B
Human papillomavirus (HPV)
Shingles (herpes-zoster virus)
26
what is a Live attenuated vaccines
contain a weakened version of the pathogen.
They are still capable of causing infection, particularly in immunocompromised patients.
27
give an example of Live attenuated vaccines
* Measles, mumps and rubella vaccine: contains all three weakened viruses
* BCG: contains a weakened version of tuberculosis
* Chickenpox: contains a weakened varicella-zoster virus
* Nasal influenza vaccine (not the injection)
* Rotavirus vaccine
* Typhoid
28
what are toxin vaccines
contain a toxin that is normally produced by a pathogen.
They cause immunity to the toxin and not the pathogen itself
29
given an example of a toxin vaccine
diphtheria
tetanus
30
What vaccines are given at 8 weeks
6 in 1 vaccine (diphtheria, tetanus, pertussis, polio, haemophilus influenzae type B (Hib) and hepatitis B)
Meningococcal type B
Rotavirus (oral vaccine)
31
what is in the 6 in 1
* diphtheria
* tetanus
* pertussis
* polio
* haemophilus influenzae type B (Hib)
* hepatitis B
'Parents Will Immunise Toddlers Because Death'
32
what vaccines are given at 12 weeks
6 in 1 vaccine (again)
Pneumococcal (13 different serotypes)
Rotavirus (again)
33
what vaccines are given at 16 weeks
6 in 1 vaccine (3/3)
Meningococcal type B (2/3)
34
what vaccines are given at 1 year
2 in 1 (haemophilus influenza type B and meningococcal type C)
Pneumococcal (again)
MMR vaccine (measles, mumps and rubella)
Meningococcal type B (again)
35
what vaccines are at 3 years 4 months
4 in 1 (diphtheria, tetanus, pertussis and polio)
MMR vaccine (again)
36
what is in the 4 in 1
diphtheria, tetanus, pertussis and polio
37
what vaccine is given at 12-13 years
Human papillomavirus (HPV) vaccine (2 doses given 6 to 24 months apart)
38
what vaccine is given at 14 years
3 in 1 (tetanus, diphtheria and polio)
Meningococcal groups A, C, W and Y
39
what is in the 3 in 1
tetanus, diphtheria and polio
40
what strains of HPV cause genital warts
6 and 11
41
what strains of HPV cause cervical cancer
16 and 18
42
what is chickenpox
caused by primary infection with varicella zoster virus
43
what is shingles
reactivation of the dormant virus in dorsal root ganglion
44
how does chickenpox present
fever initially
itchy, rash starting on head/trunk before spreading. Initially macular then papular then vesicular
systemic upset is usually mild
45
when does chickenpox infectivity continue til
infectivity continues until all the lesions are dry and have crusted over
46
what are complications of chickenpox
common - secondary bacterial infection of the lesions --> group A streptococcal
rare:
pneumonia
encephalitis (cerebellar involvement may be seen)
disseminated haemorrhagic chickenpox
arthritis, nephritis and pancreatitis may very rarely be seen
47
what is 1st disease
Measles
48
what is 2nd disease
Scarlet Fever
49
what is 3rd disease
Rubella (AKA German Measles)
50
what is 4th disease
Dukes’ Disease
51
what is 5th disease
Parvovirus B19
52
what is 6th disease
Roseola Infantum
53
what is measles
caused by the measles virus. It is highly contagious via respiratory droplets.
54
how does measles present
Koplik spots - spots inside the mouth (pathognomonic)
erythematous, maculopapular rash with flat lesions starts on face behind ears after fever then spreads to rest of body
55
how is measles managed
self resolving after 7 – 10 days of symptoms.
Children should be isolated until 4 days from onset of rash
56
what are notifiable diseases
Measles
Scarlet Fever
Rubella (AKA German Measles)
57
what are complications of measles
Otitis media
Pneumonia
Diarrhoea
Dehydration
Encephalitis
Meningitis
Hearing loss
Vision loss
Death
58
what is scarlet fever
caused by an exotoxin produced by the streptococcus pyogenes (group A strep) bacteria
59
how does scarlet fever present
red-pink, blotchy, macular rash with rough “sandpaper” skin starts on trunk and spreads
Fever: typically lasts 24 to 48 hours
Lethargy
Flushed face
Sore throat
Strawberry tongue
Cervical lymphadenopathy
60
how is scarlet fever managed
phenoxymethylpenicillin (penicillin V) for 10 days.
Children should be kept off school until 24 hours after starting antibiotics.
61
what other conditions are associated with group a strep infection
Post-streptococcal glomerulonephritis rheumatic fever
62
what is rubella
caused by the togavirus virus
highly contagious
spread by respiratory droplets
63
how does rubella present
milder erythematous macular rash compared with measles
starts on face spreads to body
mild fever, joint pain and a sore throat
lymphadenopathy
64
how is rubella managed
supportive and the condition is self limiting
Children should stay off school for at least 5 days after the rash appears.
Children should avoid pregnant women.
65
what are complications of rubella
arthritis
thrombocytopaenia
encephalitis
myocarditis
66
what can rubella in pregnancy lead to
congenital rubella syndrome, which is a triad of
* deafness
* blindness
* congenital heart disease.
67
what is Parvovirus B19
caused by the parvovirus B19
also known as fifth disease, slapped cheek syndrome and erythema infectiosum
68
how does Parvovirus B19 present
starts with mild fever, coryza and non-specific viral symptoms such as muscle aches and lethargy
After 2 – 5 days the rash appears quite rapidly as a diffuse bright red rash on both cheeks, as though they have “slapped cheeks
few days later a reticular (net-like) mildly erythematous rash affecting the trunk and limbs appears that can be raised and itchy.
69
how is parovirus b19 managed
self limiting and the rash and symptoms usually fade over 1 – 2 week
70
when is parovirus b19 infectious
infectious prior to the rash forming, but once the rash has formed they are no longer infectious and do not need to stay off school.
71
who is at risk of parovirus b19 complucations
mmunocompromised patients, pregnant women and patients with haematological conditions such as sickle cell anaemia, thalassaemia, hereditary spherocytosis and haemolytic anaemia
72
what are complications of parovirus b19
Aplastic anaemia
Encephalitis or meningitis
Pregnancy complications including fetal death
Rarely hepatitis, myocarditis or nephritis
73
what is Roseola Infantum caused by
human herpesvirus 6 (HHV-6) and less frequently by human herpesvirus 7 (HHV-7).
74
what is main complication of Roseola Infantum
febrile convulsions
75
how does Roseola Infantum present
3-5 day high fever followed by a 2 day maculopapular rash which starts on the chest and spreads to the limbs.
76
what is Staphylococcal Scalded Skin Syndrome
caused by a type of staphylococcus aureus bacteria that produces epidermolytic toxins --> protease enzymes that break down the proteins that hold skin cells together.
77
how does SSSS present
generalised patches of erythema on the skin
formation of fluid filled blisters called bullae
burst & leave very sore, erythematous skin below
78
what is Nikolsky sign
very gentle rubbing of the skin causes it to peel away.
79
what are complications of SSSS
untreated lead to sepsis and potentially death.
80
How is SSSS managed
admission and treatment with IV antibiotics.
Fluid and electrolyte balance
81
What is whooping cough
upper respiratory tract infection caused by Bordetella pertussis (a gram negative bacteria).
82
how does whooping cough present
starts with mild coryzal symptoms, a low grade fever and possibly a mild dry cough.
More severe coughing fits start after a week or more
large, loud inspiratory whoop when the coughing ends
83
what is a paroxysmal cough
Coughing fits are severe and keep building until the patient is completely out of breath.
84
how is whooping cough diagnosed
within 2-3 weeks = nasopharyngeal or nasal swab with PCR testing or bacterial culture
more than 2 weeks = anti-pertussis toxin immunoglobulin G.
85
how is whooping cough managed
notifiable disease
supportive care
within first 3 weeks = Macrolide antibiotics such as azithromycin, erythromycin and clarithromycin
close contacts = prophylactic antibiotics
86
what is a complication if whoopung cough
bronchiectasis.
87
what is TB
infectious disease caused by Mycobacterium tuberculosis, a small rod-shaped bacteria (a bacillus)
88
what stain is used for M. tuberculosis and what does it look like
Zeihl-Neelsen stain, which turns them bright red against a blue background.
acid fast bacilli
89
what are the 4 possible outcomes of TB disease course
- Immediate clearance of the bacteria (in most cases)
- Primary active tuberculosis (active infection after exposure)
- Latent tuberculosis (presence of the bacteria without being symptomatic or contagious)
- Secondary tuberculosis (reactivation of latent tuberculosis to active infection)
90
what is miliary tuberculosis
When the immune system cannot control the infection, disseminated and severe disease can develop
91
what happens in latent TB
the immune system encapsulates the bacteria and stops the progression of the disease.
92
what is secondary TB
When latent tuberculosis reactivates, and an infection develops, usually due to immunosuppression
93
what is MC site of TB infection
lungs
94
What are Extrapulmonary tuberculosis sites
Lymph nodes
Pleura
Central nervous system
Pericardium
Gastrointestinal system
Genitourinary system
Bones and joints
Skin (cutaneous tuberculosis)
95
what is a cold abscess
firm, painless abscess caused by tuberculosis usually in neck
96
what are RF for TB
* Close contact with active tuberculosis (e.g., a household member)
* Immigrants from areas with high tuberculosis prevalence
* People with relatives or close contacts from countries with a high rate of TB
* Immunocompromised (e.g., HIV or immunosuppressant medications)
* Malnutrition, homelessness, drug users, smokers and alcoholics
97
WHat is the vaccine for TB
Bacillus Calmette–Guérin (BCG)
live attenuated (weakened) Mycobacterium bovis bacteria (close relative)
98
who is TB vax offered to
increased risk of TB, such as those from areas of high TB prevalence, with close contact with TB (e.g., family members) and healthcare workers
99
how does TB present
Cough
Haemoptysis (coughing up blood)
Lethargy
Fever or night sweats
Weight loss
Lymphadenopathy
Erythema nodosum (tender, red nodules on the shins caused by inflammation of the subcutaneous fat)
Spinal pain in spinal tuberculosis (also known as Pott’s disease of the spine)
100
what are the two tests for an immune response to TB cause by previous infection, latent or actiev TB
Mantoux test
Interferon‑gamma release assay (IGRA)
101
what investigations can support TB diagnosis
Chest x-ray
Cultures
102
what is Mantoux test
injecting tuberculin into the intradermal space on the forearm.
infection creates a bleb under skin
induration of skin measured 5mm or more = positive test
103
what is Interferon-Gamma Release Assays
mixing a blood sample with antigens from the M. tuberculosis bacteria.
positive result is when interferon-gamma is released during the test.
104
what does primary TB show on XRay
patchy consolidation, pleural effusions and hilar lymphadenopathy.
105
what does Reactivated TB show on XRay
patchy or nodular consolidation with cavitation (gas-filled spaces), typically in the upper zones.
106
what does Disseminated miliary TB show on XRay
appearance of millet seeds uniformly distributed across the lung fields.
107
what are ways to collect TB culture sample
Sputum cultures (3 separate sputum samples are collected)
Mycobacterium blood cultures (require special blood culture bottle)
Lymph node aspiration or biopsy
Sputum induction with nebulised hypertonic saline
Bronchoscopy and bronchoalveolar lavage (saline is used to wash the airways and collect a sample)
108
how is latent TB treated
Isoniazid and rifampicin for 3 months
or
Isoniazid for 6 months
109
how is active TB treated
R – Rifampicin for 6 months
I – Isoniazid for 6 months
P – Pyrazinamide for 2 months
E – Ethambutol for 2 months
110
what is co prescribed with RIPE for TB
pyridoxine or vitamin B6.
111
what is SE of Rifampicin
- Red/orange discolouration of secretions, such as urine and tears.
- It is a potent inducer of the cytochrome P450 enzymes and reduces the effects of drugs metabolised by this system
112
What is SE of Isoniazid
can cause peripheral neuropathy
113
what is SE of Pyrazinamide
hyperuricaemia (high uric acid levels), resulting in gout and kidney stones.
114
WHat is SE of Ethambutol
colour blindness and reduced visual acuity.
115
what TB drug is NOT associated with hepatotoxicity
Ethambutol <3
116
what is HIV
human immunodeficiency virus
117
what is AIDS
acquired immunodeficiency syndrome
end stage HIV
118
what type of virus is HIV
RNA retrovirus
119
what is the pathophysiology of HIV
virus enters and destroys the CD4 T helper cells.
initial seroconversion flu
120
what are AIDs defining illnesses
Kaposi’s sarcoma
Pneumocystis jirovecii pneumonia (PCP)
Cytomegalovirus infection
Candidiasis (oesophageal or bronchial)
Lymphomas
Tuberculosis
121
how is HIv spread
- Unprotected anal, vaginal or oral sexual activity
- Mother to child at any stage of pregnancy, birth or breastfeeding. This is referred to as vertical transmission.
- Mucous membrane, blood or open wound exposure to infected blood or bodily fluids.
passed on through blood, semen, vaginal fluid, anal mucus and breast milk,
122
When is a normal vaginal delivery recommended for HIV + women
viral load < 50 copies / ml
123
When is a Caesarean section considered for HIV + women
> 50 copies copies / ml and in all women with > 400 copies / ml
124
what medication is given during. c section is viral load unknown of HIV + mother or >10000 coplies/ml
IV zidovudine
125
What Prophylaxis treatment may be given to the baby when HIV + mother viral load is < 50 copies per ml
zidovudine for 4 weeks
126
What Prophylaxis treatment may be given to the baby when HIV + mother viral load is >50 copies per ml
zidovudine, lamivudine and nevirapine for 4 weeks
127
when is breastfeeding recommended for mothers with HIV
never
128
what are two options for HIV testing
HIV antibody screen
HIV viral load
129
what is HIV antibody screen:
tests whether the immune system has created antibodies due to exposure to the HIV virus
standard screening
can give false positive
130
what is HIV viral load
tests directly for viruses in the blood
never be falsely positive
131
what can cause false positive in hiv antibody tets
can be positive in infants who do not have HIV for up to 18 months of age. This is due to maternal antibodies that have crossed the placenta during pregnancy.
132
when is HIv tested
Babies to HIV positive parents
When immunodeficiency is suspected, for example where there are unusual, severe or frequent infections
Young people who are sexually active can be offered testing if there are concerns
Risk factors such as needle stick injuries, sexual abuse or IV drug use
133
how is HIV managed
- Antiretroviral therapy (ART) to suppress the HIV infection
- Normal childhood vaccines, avoiding or delaying live vaccines if severely immunosuppressed.
- Prophylactic co-trimoxazole (Septrin) for children with low CD4 counts, to protect against pneumocystis jirovecii pneumonia (PCP)
- Treatment of opportunistic infections
134
what is the aim of antiretroviral therapy (ART)
chieve a normal CD4 count and undetectable viral load.
135
what should paediatric HIV multidisciplinary team be involved in
Regular follow up to monitor growth and development
Dietician input for nutritional support when required
Parental education about the condition
Disclosing the diagnosis to the child is often delayed until they are mature enough
Psychological support
Specific sex education in relation to HIV when appropriate
136
what is Meningitis
inflammation of the meninges. The meninges are the lining of the brain and spinal cord
137
what is Neisseria meningitidis
gram-negative diplococcus bacteria
commonly known as meningococcus
138
what is Meningococcal septicaemia
meningococcus bacterial infection in the bloodstream.
139
what does non-blanching rash in Meningitis indicate
the infection has caused disseminated intravascular coagulopathy (DIC) and subcutaneous haemorrhages
140
what is Meningococcal meningitis
the bacteria is infecting the meninges and the cerebrospinal fluid around the brain and spinal cord
141
what are the MC causes of bacterial meningitis in children and adults
Neisseria meningitidis (meningococcus) and Streptococcus pneumoniae (pneumococcus).
142
what is the MC cause of meningitis in neonates
group B strep (GBS).
143
how does meningitis present
fever, neck stiffness, vomiting, headache, photophobia, altered consciousness and seizures
non-blanching rash
144
how do neonates and babies present with meningitis
non-specific signs and symptoms, such as hypotonia, poor feeding, lethargy, hypothermia and a bulging fontanell
145
when does NICE recommen a LP as investigation in children
- Under 1 month presenting with fever
- 1 to 3 months with fever and are unwell
- Under 1 year with unexplained fever and other features of serious illness
146
what is kernig test
lying the patient on their back, flexing one hip and knee to 90 degrees and then slowly straightening the knee whilst keeping the hip flexed at 90 degrees
meningitis = spinal pain or resistance to movement.
147
what is Brudzinski’s test
ying the patient flat on their back and gently using your hands to lift their head and neck off the bed and flex their chin to their chest.
meningitis = patient to involuntarily flex their hips and knees.
148
how is meningitis managed in the community
IM benzylpenicillin
149
how is meningitis managed in the hospital
Under 3 months – cefotaxime plus amoxicillin (for listeria)
Above 3 months – ceftriaxone
150
how is meningitis investigated
blood culture
lumpar puncture
meningococcal PCR
Viral PCR
151
what prophylaxis is given for meningitis
single dose of ciprofloxacin
close contact within 7 days of symptoms
152
what are common viral causes of meningitis
herpes simplex virus (HSV), enterovirus and varicella zoster virus (VZV)
153
how is viral meningitis treated
Aciclovir
154
what are the LP results for bacterial meningitis
Appearance - cloudy
Protein - high
Glucose - low
White Cell Count - high neutrophils
Culture - bacteria
155
what are the LP results for viral meningitis
Appearance - clear
Protein - mild raised or normal
Glucose -normal
White Cell Count - high lymphocytes
Culture - negative
156
what are complications of meningitis
Hearing loss is a key complication
Seizures and epilepsy
Cognitive impairment and learning disability
Memory loss
Cerebral palsy, with focal neurological deficits such as limb weakness or spasticity
157
at what level is a LP taken at
L3 – L4
158
what are LP sample tested for
bacterial culture, viral PCR, cell count, protein and glucose
159
what is given in addition to Abx to reduce frequency and severity of hearing and neurological loss
Dexamethasone is given 4 times daily for 4 days to children over 3 months
160
what is Encephalitis
inflammation of the brain. This can be the result of infective or non-infective causes.
non infective = autoimmune
161
what is MC cause of Encephalitis in children
herpes simple type 1 (HSV-1) from cold sores.
162
what is MC cause of Encephalitis in neonates
herpes simplex type 2 (HSV-2) from genital herpes, contracted during birth.
163
what are other viral causes of Encephalitis
varicella zoster virus (VZV) -> chickenpox
cytomegalovirus -> immunodeficiency
Epstein-Barr virus -> infectious mononucleosis
enterovirus
adenovirus
influenza virus.
164
how does Encephalitis present
Altered consciousness
Altered cognition
Unusual behaviour
Acute onset of focal neurological symptoms
Acute onset of focal seizures
Fever
165
how are children with suspected Encephalitis investigated
Lumbar puncture -> cell count, protein and glucose levels, Gram stain, bacterial culture, viral PCR testing
MRI scan
EEG recording
HIV testing
166
when is LP CI
GCS below 9, haemodynamically unstable, active seizures or post-ictal.
167
how is herpes simplex virus (HSV) and varicella zoster virus (VZV) encephalitis treated
Aciclovir
168
how is cytomegalovirus (CMV) encephalitis treated
Ganciclovir
169
what is performed before stopping antivirals for encephalitis
Repeat lumbar puncture
Followup, support and rehabilitation is required after encephalitis
170
what are complications of encephalitis
Lasting fatigue and prolonged recovery
Change in personality or mood
Changes to memory and cognition
Learning disability
Headaches
Chronic pain
Movement disorders
Sensory disturbance
Seizures
Hormonal imbalance
171
what is Impetigo
superficial bacterial skin infection, usually caused by the staphylococcus aureus bacteria
Impetigo is contagious and children should be kept off school during the infection.
172
how is Impetigo classified
non-bullous or bullous.
173
what is non bullous Impetigo
typically occurs around the nose or mouth.
The exudate from the lesions dries to form a “golden crust”
rarely causes systemic symptoms
174
how is localised non bullous Impetigo treated
1st line antiseptic cream (hydrogen peroxide 1% cream)
175
how is wide spread non bullous Impetigo treated
* oral flucloxacillin
* oral erythromycin if penicillin-allergic
176
what is advice to stop spread of Impetigo
not touching or scratching the lesions, hand hygiene and avoiding sharing face towels and cutlery
off school until all the lesions have healed or they have been treated with antibiotics for at least 48 hours
177
what is Bullous impetigo
staphylococcus aureus bacteria produce epidermolytic toxins that break down skin cells causing fluid filled vesicles to form grow and cause golden crust to form
+ systemic symtoms - feverish and generally unwell
178
who is Bullous impetigo most commin
neonates and children under 2 years
179
how is Bullous impetigo investigated
Swabs of the vesicles can confirm the diagnosis, bacteria and antibiotic sensitivities.
180
what can severe bullous impetigo infection lead to
staphylococcus scalded skin syndrome.
181
how is bullous impetigo treated
oral or IV flucloxacillin
182
what are complications of impetigo
Cellulitis if the infection gets deeper in the skin
Sepsis
Scarring
Post streptococcal glomerulonephritis
Staphylococcus scalded skin syndrome
Scarlet fever
183
what is 1st line treatment for mild to moderate Oral candidiasis
Topical antifungals:
Nystatin suspension
Miconazole gel
184
what is 1st line treatment for severe Oral candidiasis
Oral fluconazole
185
what are Rf for Oral candidiasis
DM
denture use
inhaled ICS
immunicompromised
186
what is Hand, foot and mouth disease caused by
coxsackie A virus
187
how does Hand, foot and mouth disease present
starts with typical viral upper respiratory tract symptoms such as tiredness, sore throat, dry cough and raised temperatur
1-2 days later small mouth ulcers appear, followed by blistering red spots across the body
Painful mouth ulcers, particularly on the tongue are also a key feature
188
how is how does Hand, foot and mouth disease managed
no treatment for hand, foot and mouth disease.
Management is supportive, with adequate fluid intake and simple analgesia such as paracetamol if required
189
what are complications of Hand, foot and mouth disease
Dehydration
Bacterial superinfection
Encephalitis
190
how long should it take for Hand, foot and mouth disease to resolve
esolve spontaneously without treatment after a week to 10 days
191
what is an allergy
hypersensitivity of the immune system to allergens.
192
what are allergens
proteins that the immune system recognises as foreign and potential harmful, leading to an allergic immune response
193
what are antigens
proteins that can be recognised by the immune system.
194
what is atopy
predisposition to having hypersensitivity reactions to allergens
195
what are atopic conditions
eczema, asthma, hayfever, allergic rhinitis and food allergies.
196
what is the leading theory on orugin of allergies
skin sensitisation theory
197
what is skin sensitisation theory
two main contributors to a child developing an allergy to a food:
1. There is a break in the infant’s skin (from eczema or a skin infection) that allows allergens, such as peanut proteins, from the environment to cross the skin and react with the immune system.
2. The child does not have contact with that allergen from the gastrointestinal tract, and there is an absence of GI exposure to the allergen.
198
what conditions are a result of hypersensitivity reactions
Asthma
Atopic eczema
Allergic rhinitis
Hayfever
Food allergies
Animal allergies
199
what is type 1 Coombs and Gell classification
Antigen reacts with IgE bound to mast cells
200
Give an example of a type 1 Coombs and Gell classification
Anaphylaxis
Atopy (e.g. asthma, eczema and hayfever)
201
what is type 2 Coombs and Gell classification
IgG or IgM binds to antigen on cell surface and activate the complement system
202
Give an example of a type 2 Coombs and Gell classification
haemolytic disease of the newborn
ITP
Pernicious anaemia
Goodpastures
203
what is type 3 Coombs and Gell classification
Free antigen and antibody (IgG, IgA) combine and accumulate and cause damage to local tissues.
204
Give an example of a type 3 Coombs and Gell classification
systemic lupus erythematosus (SLE)
Post-streptococcal glomerulonephritis
Henoch-Schönlein purpura (HSP)
205
what is type 4 Coombs and Gell classification
hypersensitivity T-cell mediated
206
Give an example of a type 4 Coombs and Gell classification
MS
TB
Guillain-Barre syndrome
organ transplant rejection
207
what are 3 ways of test for allergy
Skin prick testing
RAST testing, which involves blood tests for total and specific immunoglobulin E (IgE)
Food challenge testing
208
which allergy tests are unreliable and misleading
Skin prick testing and RAST testing assess sensitisation and not allergy.
= makes the unreliable and misleading
209
what is the gold standard investigation for diagnosing allergy
Foot challenge testing
210
what is Skin Prick Testing
1. A drop of each allergen solution is placed at marked points along the patch of skin, along with a water control and a histamine control.
2. A fresh needle is used to make a tiny break in the skin at the site of each allergen.
3. After 15 minutes, the size of the wheals to each allergen are assessed and compared to the controls.
211
what is patch testing
most helpful in determining an allergic contact dermatitis in response to a specific allergen NOT food allergies
1. A patch containing the allergen is placed on the patient’s skin. The patch can either contain a specific allergen, or a grid of lots of allergens as a screening tool.
2. After 2 – 3 days the skin reaction to the patch is assessed.
212
what is RAST testing
measures the total and allergen specific IgE quantities in the patient’s blood sample.
213
what is food challenge
child is gradually given increasing quantities of an allergen to assess the reaction, starting with almost non-existent quantities diluted further in other foods, for example mixing a small amount of peanut into a bar of chocolate.
214
how are allergies managed
* Establishing the correct allergen is essential
* Avoidance of that allergen
* Avoiding foods that trigger reactions
* Regular hoovering and changing sheets and pillows in patients that are allergic to house dust mites
* Staying in doors when the pollen count is high
* Prophylactic antihistamines are useful when contact is inevitable, for example hayfever and allergic rhinitis
* Patients at risk of anaphylactic reactions should be given an adrenalin auto-injector
215
what is immunotherapy for allergies
gradually exposing the patients to allergens over months with the aim of reducing their reaction to certain foods or allergens.
216
what is the management of allergies follwoing exposure
- Antihistamines (e.g. cetirizine)
- Steroids (e.g. oral prednisolone, topical hydrocortisone or IV hydrocortisone)
- Intramuscular adrenalin in anaphylaxis
217
what is Allergic rhinitis
IgE-mediated type 1 hypersensitivity reaction.
Environmental allergens cause an allergic inflammatory response in the nasal mucosa
218
when can Allergic rhinitis occur
Seasonal, for example hay fever
Perennial (year round), for example house dust mite allergy
Occupational, associated with the school or work environment
219
how does Allergic rhinitis present
Runny, blocked and itchy nose
Sneezing
Itchy, red and swollen eyes
220
how is Allergic rhinitis investigated
diagnosis usually history
Skin prick testing - pollen, animals and house dust mite allergy
221
what can trigger Allergic rhinitis
- Tree pollen or grass allergy
- House dust mites and pets
- Pets can
- Other allergens lead to symptoms after exposure (e.g. mould)
222
what are Non-sedating antihistamines for Allergic rhinitis
cetirizine, loratadine and fexofenadine
223
what are sedating antihistamines for Allergic rhinitis
chlorphenamine (Piriton) and promethazine
224
what are nasal corticosteroid sprays for Allergic rhinitis
fluticasone and mometasone
225
what is Anaphylaxis
life-threatening medical emergency
severe type 1 hypersensitivity reaction
226
what is the pathophysiology of Anaphylaxis
- Immunoglobulin E (IgE) stimulates mast cells to rapidly release histamine and other pro-inflammatory chemicals.
- This is called mast cell degranulation.
- This causes a rapid onset of symptoms, with airway, breathing and/or circulation compromise
227
what are the rapid onset of allergic symptoms
Urticaria
Itching
Angio-oedema, with swelling around lips and eyes
Abdominal pain
228
what additional symptoms indicate anaphylaxis
Shortness of breath
Wheeze
Swelling of the larynx, causing stridor
Tachycardia
Lightheadedness
Collapse
229
how is anaphylaxis initially assessed
A – Airway: Secure the airway
B – Breathing: Provide oxygen if required. Salbutamol can help with wheezing.
C – Circulation: Provide an IV bolus of fluids
D – Disability: Lie the patient flat to improve cerebral perfusion
E – Exposure: Look for flushing, urticaria and angio-oedema
230
how is anaphylaxis treated
Intramuscular adrenalin, repeated after 5 minutes if required
Antihistamines, such as oral chlorphenamine or cetirizine
231
how is anaphylaxis managed after the event
- admitted to watch for biphasic reactions (2nd anaphylactic reaction after successful treatment of the first)
- serum mast cell tryptase within 6 hours of the event.
Education and follow-up of the family and child is essential
* how to avoid allergens and how to spot the signs of anaphylaxis
* trained in basic life support
* how to use an adrenalin auto-injector.
232
what are Indications for an Adrenalin Auto-Injector
given to all children and adolescents with anaphylactic reactions.
children with generalised allergic reactions (without anaphylaxis) with certain risk factors
- Asthma requiring inhaled steroids
- Poor access to medical treatment
- Adolescents
- Nut or insect sting allergies
- Significant co-morbidities, such as cardiovascular disease
233
how is an Adrenalin Auto-Injector used
1. Prepare the device by removing the safety cap on the non-needle end
2. Grip the device with the needle end pointing downwards.
3. Administer the injection by firmly jabbing the device into the outer portion of the mid thigh until the device clicks.
4. Remove the device and gently massage the area for 10 seconds.
5. Phone an emergency ambulance. A second dose may be given (with a new pen) after 5 mins
234
how is Anaphylaxis confirmed
measuring the serum mast cell tryptase within 6 hours of the event
235
when is tryptase released
during mast cell degranulation
236
what is Urticaria
hives
small itchy lumps that appear on the skin
may be associated with a patchy erythematous rash
localized or widespread
237
what is the pathophysiology of Urticaria
caused the release of histamine and other pro-inflammatory chemicals by mast cells in the skin.
allergic reaction in acute urticaria or an autoimmune reaction in chronic idiopathic urticaria.
238
what causes 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)
239
what is acute urticaria
typically triggered by something that stimulates the mast cells to release histamine.
240
what is chronic urticaria
autoimmune condition, where autoantibodies target mast cells and trigger them to release histamines and other chemicals.
241
what is Chronic idiopathic urticaria
recurrent episodes of chronic urticaria without a clear underlying cause or trigger.
242
what can trigger Chronic inducible urticaria
Sunlight
Temperature change
Exercise
Strong emotions
Hot or cold weather
Pressure (dermatographism)
243
what is Autoimmune urticaria
chronic urticaria associated with an underlying autoimmune condition, such as systemic lupus erythematosus.
244
how is urticaria managed
Antihistamines
chronic 1st = Fexofenadine
Oral steroids for severe flares
245
what specialist treatment can be considered for severe urticaria
Anti-leukotrienes such as montelukast
Omalizumab, which targets IgE
Cyclosporin
246
what is Eczema
chronic atopic condition caused by defects in the normal continuity of the skin barrier, leading to inflammation in the skin
247
how does Eczema present
presents in infancy with dry, red, itchy and sore patches of skin over the flexor surfaces (the inside of elbows and knees) and on the face and neck
248
how is Eczema maintained
emollients
avoid activities that break down the skin barrier, such as bathing in hot water, scratching or scrubbing their skin and using soaps and body washes that remove the natural oils in the skin
249
how are Eczema flares treated
thicker emollients, topical steroids, “wet wraps” (covering affected areas in a thick emollient and applying a wrap to keep moisture locked in overnight) and treating any complications such as bacterial or viral infections.
250
what are specialist treatments in severe eczema
- zinc impregnated bandages
- topical tacrolimus
- phototherapy
- systemic immunosuppressants, such as oral corticosteroids, methotrexate and azathioprine.
251
what are Thin cream Emollients
E45
Diprobase cream
Oilatum cream
Aveeno cream
Cetraben cream
Epaderm cream
252
what are thick greasy Emollients
50:50 ointment (50% liquid paraffin)
Hydromol ointment
Diprobase ointment
Cetraben ointment
Epaderm ointment
253
what is the steroid ladder for eczema
Mild: Hydrocortisone 0.5%, 1% and 2.5%
Moderate: Eumovate (clobetasone butyrate 0.05%)
Potent: Betnovate (betamethasone 0.1%)
Very potent: Dermovate (clobetasol propionate 0.05%)
254
what is the general steroid rule for eczema
use the weakest steroid for the shortest period required to get the skin under control.
The thicker the skin, the stronger the steroid required.
255
how are bacterial infections in eczema managed
MC organism = staphylococcus aureus
Tx = flucloxacillin
256
what is Stevens-Johnson Syndrome
disproportional immune response causes epidermal necrosis, resulting in blistering and shedding of the top layer of skin
257
what medication can cause Stevens-Johnson Syndrome
Anti-epileptics
Antibiotics
Allopurinol
NSAIDs
258
what infections can cause Stevens-Johnson Syndrome
Herpes simplex
Mycoplasma pneumonia
Cytomegalovirus
HIV
259
How does Stevens-Johnson Syndrome present
- start with non-specific symptoms of fever, cough, sore throat, sore mouth, sore eyes and itchy skin
- develop a purple or red rash that spreads across the skin and starts to blister.
- blistering skin breaks away and shed leaving raw skin
260
how is Stevens-Johnson Syndrome managed
medical emergency
supportive care
Tx = steroids, immunoglobulins and immunosuppressant
261
what condition is similar to Stevens-Johnson Syndrome but covers larger part of body
toxic Epidermal Necrolysis
262
what are complications of Stevens-Johnson Syndrome
Secondary infection
Permanent skin damage
Visual complications:
263
what do B cells do
responsible for producing antibodies
specific immunity
264
what is selective Immunoglobulin A Deficiency
MC immunoglobulin deficiency
IgA = LOW
IgG = normal
IgM = normal
265
where is IgA present
secretions of the mucous membranes, such as saliva, respiratory tract secretions, GI tract secretions, tears and sweat.
protects against opportunistic infections
266
when is it important to test for total immunoglobulin A levels
in coeliac disease
267
what is Common Variable Immunodeficiency
caused by a genetic mutation in the genes coding for components of B cell
unable to develop immunity to infections or vaccination
IgG = LOW
IgA = LOW
IgM = normal
268
how does Common Variable Immunodeficiency present
recurrent respiratory tract infections, typically leading to chronic lung disease over time.
269
what conditions are patients with Common Variable Immunodeficiency prone to
rheumatoid arthritis, and cancers such as non-Hodgkins lymphoma
270
how are Common Variable Immunodeficiency managed
regular immunoglobulin infusions
271
what is X-linked Agammaglobulinaemia
X-linked recessive condition
results in abnormal B cell development and deficiency in all classes of immunoglobulins.
