paeds 2 ? Flashcards
triad of depression
Low mood
Anhedonia, a lack of pleasure in activities
Low energy
depression symptoms in youths
Low mood Anhedonia, a lack of pleasure in activities Low energy Anxiety and worry Clinginess Irritability Avoiding social situations (e.g. school) Hopelessness about the future Poor sleep, particularly early morning waking Poor appetite or over eating Poor concentration Physical symptoms such as abdominal pain
conservative management of depression
watchful waiting and advice about healthy habits, such as healthy diet, exercise and avoiding alcohol and cannabis.
moderate to severe depression treatment first line
Psychological therapy as the first line treatment with cognitive behavioural therapy, non-directive supportive therapy, interpersonal therapy and family therapy
first line antidepressant for depression in youths
Fluoxetine is the first line antidepressant in children, starting at 10mg and increasing to a maximum of 20mg
second line antidepressants for youth depression
Sertraline and citalopram
medical treatment timeline for depression
continue 6 months after remission is achieved
severity of anxiety can be assessed through
GAD-7 anxiety questionnaire, as well as co-morbidity and environmental triggers
mild anxiety treatment
watchful waiting and advice about self-help strategies (e.g. meditation), diet, exercise and avoiding alcohol, caffeine and drugs.
moderate to severe anxiety treatment
Counselling
Cognitive behavioural therapy
Medical management. Usually an SSRI such as sertraline is considered.
obsessions are
unwanted and uncontrolled thoughts and intrusive images
compulsions are
repetitive actions the person feels they must do, generating anxiety if they are not done.
features of autistic social interaction
Lack of eye contact Delay in smiling Avoids physical contact Unable to read non-verbal cues Difficulty establishing friendships Not displaying a desire to share attention
features of communication in autistics
Delay, absence or regression in language development
Lack of appropriate non-verbal communication such as smiling, eye contact, responding to others and sharing interest
Difficulty with imaginative or imitative behaviour
Repetitive use of words or phrases
behavioural features in autistic
Greater interest in objects, numbers or patterns than people
Stereotypical repetitive movements. There may be self-stimulating movements that are used to comfort themselves, such as hand-flapping or rocking.
Intensive and deep interests that are persistent and rigid
Repetitive behaviour and fixed routines
Anxiety and distress with experiences outside their normal routine
Extremely restricted food preferences
what key part of ADHD helps differentiate it from an enviromental problem?
consistent across all various settings
features of ADHD
Very short attention span
Quickly moving from one activity to another
Quickly losing interest in a task and not being able to persist with challenging tasks
Constantly moving or fidgeting
Impulsive behaviour
Disruptive or rule breaking
what is the type of medication used for treatment of ADHD
central nervous system stimulants.
examples of medication used in ADHD
Methylphenidate (“Ritalin“)
Dexamfetamine
Atomoxetine
pathology of anorexia
the person feel they are overweight despite evidence of normal or low body weight. It involves obsessively restricting calorie intake with the intention of losing weight.
features of anorexia nervosa
Excessive weight loss Amenorrhoea Lanugo hair is fine, soft hair across most of the body Hypokalaemia Hypotension Hypothermia Changes in mood, anxiety and depression Solitude
cardiac complications of anorexia include
arrhythmia, cardiac atrophy and sudden cardiac death.
the teenage girl with a normal body weight that presents with swelling to the face or under the jaw (salivary glands), calluses on the knuckles and alkalosis on a blood gas. The presenting complaint may be abdominal pain or reflux.. what is the underlying problem?
bulimia nervosa
features of bulimia nervosa?
alkalosis, due to vomiting hydrochloric acid from the stomach
Hypokalaemia
Erosion of teeth
Swollen salivary glands
Mouth ulcers
Gastro-oesophageal reflux and irritation
Calluses on the knuckles where they have been scraped across the teeth. This is called Russell’s sign.
binge eating disorder may involve
A planned binge involving “binge foods” Eating very quickly Unrelated to whether they are hungry or not Becoming uncomfortably full Eating in a “dazed state”
high risk for refeeding syndrome are those
if they have a BMI below 20 and have had little to eat for the past 5 days.
pathology behind refeeding syndrome
Metabolism in the cells and organs dramatically slows during prolonged periods of malnutrition. As the starved cells start to process glucose, protein and fats again they use up magnesium, potassium and phosphorus.
refeeding syndrome protocol
Slowly reintroducing food with restricted calories
Magnesium, potassium, phosphate and glucose monitoring along with other routine bloods
Fluid balance monitoring
ECG monitoring may be required in severe cases
Supplementation with electrolytes and vitamins, particularly B vitamins and thiamine
anxiety personality disorders
avoidant, dependent and obsessive.
Avoidant personality disorder features
severe anxiety about rejection or disapproval and avoidance of social situations or relationships.
Dependent personality disorder features
heavy reliance on others to make decisions and take responsibility for their lives, taking a very passive approach.
Obsessive compulsive personality disorder features
features unrealistic expectations of how things should be done by themselves and others, and catastrophising about what will happen if these expectations are not met.
Paranoid personality disorder features
features difficulty in trusting or revealing personal information to others.
Schizoid personality disorder features
features a lack of interest or desire to form relationships with others and feelings that this is of no benefit to them.
emotional impulsive personality disorder examples
borderline personality disorder, histrionic, narcissistic
Borderline personality disorder features
fluctuating strong emotions and difficulties with identity and maintaining healthy relationships.
Histrionic personality disorder features
features the need to be at the centre of attention and having to perform for others to maintain that attention.
Narcissistic personality disorder features
features feelings that they are special and need others to recognise this or else they get upset. They put themselves first.
examples of suspicious personality disorders
paranoid, schizoid and schizotypal.
key management of choice for a personality disorder
Cognitive behavioural therapy (CBT) and psychotherapy
Copropraxia refers too
involves making obscene gestures
Coprolalia refers too
involves saying obscene words
Echolalia refers too
involves repeating other people’s words
troublesome tics may be treated with
Habit reversal training
Exposure with response prevention
Medications may be tried in very severe cases, usually with antipsychotic medications
Fetal haemoglobin subunits are
two alpha and two gamma subunits.
adult haemoglobin subunits are
two alpha and two beta subunits.
foetal or adult haemoglobin has greater affinity?
foetal.
at birth the haemoglobin ratio is
At birth, around half the haemoglobin produced is HbF and half is HbA
what drug can be used to increase production of foetal haemoglobin in patients with sickle cell anaemia?
Hydroxycarbamide
foetal haemoglobin doesnt sickle because
is no beta subunit in the structure.
normal haemoglobin at birth?
150 – 235 grams/litre
normal haemoglobin at 2 months - 6 years
110 – 140 grams/litre
female haemoglobin 12-18
120 – 160 grams/litre
normal haemoglobin 12-18 male
130 -160 grams/litre
common cause on anaemia in infancy is
Physiologic anaemia of infancy
other causes of anaemia in infants is
Anaemia of prematurity
Blood loss
Haemolysis
Twin-twin transfusion
haemolytic causes of anaemia
Haemolytic disease of the newborn (ABO or rhesus incompatibility)
Hereditary spherocytosis
G6PD deficiency
normal dip in haemoglobin in infants occurs around
six to nine weeks
phsyiological anaemia of infancy is due to
High oxygen delivery to the tissues caused by the high haemoglobin levels at birth cause negative feedback. Production of erythropoietin by the kidneys is suppressed and subsequently there is reduced production of haemoglobin by the bone marrow.
common causes of Anaemia in older children is
Iron deficiency anaemia secondary to dietary insufficiency. This is the most common cause overall.
Blood loss, most frequently from menstruation in older girls
common cause of global chronic anaemia is
Worldwide, a common cause of blood loss causing chronic anaemia and iron deficiency is helminth infection, with roundworms, hookworms or whipworms.
causes of microcytic anaemia
T – Thalassaemia A – Anaemia of chronic disease I – Iron deficiency anaemia L – Lead poisoning S – Sideroblastic anaemia
causes of normocytic anaemia
A – Acute blood loss A – Anaemia of Chronic Disease A – Aplastic Anaemia H – Haemolytic Anaemia H – Hypothyroidism
causes of macrocytic megaloblastic anaemia
B12 deficiency
Folate deficiency
causes of normoblastic macrocytic anamia
Alcohol Reticulocytosis (usually from haemolytic anaemia or blood loss) Hypothyroidism Liver disease Drugs such as azathioprine
symptoms of anaemia
Tiredness Shortness of breath Headaches Dizziness Palpitations Worsening of other conditions
specific symptoms of iron deficiency anaemia
pica and hair loss
general signs of anaemia
Pale skin
Conjunctival pallor
Tachycardia
Raised respiratory rate
specific signs of anaemia
koilonychia, angular chelitis, atrophic glossitis, brittle hair and nails, jaundice or bone deformities (thalassaemia)
initial investigations for anaemia
Full blood count for haemoglobin and MCV Blood film Reticulocyte count Ferritin (low iron deficiency) B12 and folate Bilirubin (raised in haemolysis) Direct Coombs test (autoimmune haemolytic anaemia) Haemoglobin electrophoresis (haemoglobinopathies)
iron is absorbed in the
duodenum and jejunum.
what form is iron absorbed in
ferrous (Fe2+) due to stomach acid.
ferric ions bind to what carrier?
transferrin
total iron binding capacity related to the amount of?
transferrin
transferring saturation =
Serum Iron / Total Iron Binding Capacity
extra ferritin may be released when there is
inflammation.
normal total iron binding capacity
54 – 75 μmol/L
what may give the impression of iron overload?
acute liver damage
what type of leukemia is most common?
Acute lymphoblastic leukaemia (ALL)
Acute lymphoblastic leukaemia commonly peaks at age
2-3
Acute myeloid leukaemia (AML) peaks age
under 2 years
what syndromes increases risk of leukaemia
Down’s syndrome
Kleinfelter syndrome
Noonan syndrome
Fanconi’s anaemia
presentation of leukaemia
Persistent fatigue Unexplained fever Failure to thrive Weight loss Night sweats Pallor (anaemia) Petechiae and abnormal bruising (thrombocytopenia) Unexplained bleeding (thrombocytopenia) Abdominal pain Generalised lymphadenopathy Unexplained or persistent bone or joint pain Hepatosplenomegaly
refer any child to haemotology for oncological assessmen if presenting with
unexplained petechiae or hepatomegaly
if leukaemia is suspected what test should be urgently performed?
FBc <48 hours
investigations for diagnosis of leukaemia should be
Full blood count, which can show anaemia, leukopenia, thrombocytopenia and high numbers of the abnormal WBCs
Blood film, which can show blast cells
Bone marrow biopsy
Lymph node biopsy
staging investigations for leukaemia include
Chest xray
CT scan
Lumbar puncture
Genetic analysis and immunophenotyping of the abnormal cells
therapies for leukaemia are
chemotherapy.
Other therapies:
Radiotherapy
Bone marrow transplant
Surgery
key differential haematoligcal for non blanching rash
leukaemia or idiopathic thrombocytopenic purpura
ITP is an example of what type of hypersensitivity?
type II hypersensitivity reaction. It is caused by the production of antibodies that target and destroy platelets.
presentation of ITP is
Often there is a history of a recent viral illness. The onset of symptoms occurs over 24 – 48 hours:
Bleeding, for example from the gums, epistaxis or menorrhagia
Bruising
Petechial or purpuric rash, caused by bleeding under the skin
petechiae size
~1mm
purpura size
3-10mm
ecchymoses size
> 10mm
ix for ITP
urgent full blood count for the platelet count.
for severe bleeds with ITP treatment should be
may be required if the patient is actively bleeding or severe thrombocytopenia (platelets below 10):
Prednisolone
IV immunoglobulins
Blood transfusions if required
Platelet transfusions only work temporarily
sickle cell anaemia genetic transmission is via
autosomal recessive
what chromosome is effected with sickle cell anaemia
chromosome 11
complications of sickle cell anaemia
Anaemia Increased risk of infection Stroke Avascular necrosis in large joints such as the hip Pulmonary hypertension Painful and persistent penile erection (priapism) Chronic kidney disease Sickle cell crises Acute chest syndrome
general management of sickle cells anaemia?
Avoid dehydration and other triggers of crises
Ensure vaccines are up to date
Antibiotic prophylaxis to protect against infection, usually with penicillin V (phenoxymethypenicillin)
hydroxycarbamide
curative option for sickle cell anaemia?
bone marrow transplant
supportive management for a sickle cell crisis
Have a low threshold for admission to hospital
Treat any infection
Keep warm
Keep well hydrated (IV fluids may be required)
Simple analgesia such as paracetamol and ibuprofen
vaso-occlusive crisis may cause what in men?
priapism in men by trapping blood in the penis, causing a painful and persistent erection.
splenic sequestration crisis refers too
red blood cells blocking blood flow within the spleen. This causes an acutely enlarged and painful spleen.
complication of splenic sequestration crisis is
circulatory collapse.
sickle cell aplastic crisis may be causes by
parvovirus B19
aplastic crisis refers too
temporary loss of the creation of new blood cells.
diagnosis of sickle cell acute chest syndrome requires.
Fever or respiratory symptoms, with:
New infiltrates seen on a chest xray
Tx for sickle cell acute chest syndrome is
Antibiotics or antivirals for infections
Blood transfusions for anaemia
Incentive spirometry using a machine that encourages effective and deep breathing
Artificial ventilation with NIV or intubation may be required
both thalassaemia’s genetic inheritance are
autosomal recessive
signs and symptoms of thalassaemia
Microcytic anaemia (low mean corpuscular volume) Fatigue Pallor Jaundice Gallstones Splenomegaly Poor growth and development Pronounced forehead and malar eminences
diagnosis of thalassaemia is through
Full blood count shows a microcytic anaemia.
Haemoglobin electrophoresis is used to diagnose globin abnormalities.
DNA testing
risk of treatment with thalassaemia?
iron overload requiring iron chelation therapy
alpha thalassaemia is caused by defects on chromosome
16
beta Thalassaemia Minor means
they have microcytic anaemia with one normal beta and one abnormal beta gene
beta Thalassaemia Intermedia means
This can be either two defective genes or one defective gene and one deletion gene.
beta thalassaemia major means
homozygous for the deletion genes.
hereditary spherocytosis genetic transmission
autosomal dominant
presentation of hereditary spherocytosis
Jaundice
Anaemia
Gallstones
Splenomegaly
crises that may arise from hereditary spherocytosis
haemolytic, or aplastic
diagnosis of hereditary spherocytosis is through
family history and clinical features, along with spherocytes on the blood film. The mean corpuscular haemoglobin concentration (MCHC) is raised on a full blood count. Reticulocytes will be raised
management of hereditary spherocytosis is
Treatment is with folate supplementation and splenectomy. Removal of the gallbladder (cholecystectomy) may be required if gallstones are a problem. Transfusions may be required during acute crises.
a patient that becomes jaundice and anaemic after eating broad beans, developing an infection or being treated with antimalarial medications. The underlying diagnosis might be
G6PD deficiency
G6PD genetic transmission is
x-linked recessive
role of G6PD enzyme is
protect cells from damage by reactive oxygen species that may cause haemolysis during period of acute stress.
G6PD presentation
neonatal jaundice.
Other features of the condition are:
Anaemia
Intermittent jaundice, particularly in response to triggers
Gallstones
Splenomegaly
G6PD on blood film may show
Heinz bodies may be seen on a on blood film. Heinz bodies are blobs of denatured haemoglobin (“inclusions”) seen within the red blood cells.
diagnosis of G6PD may be through
enzyme assay
the skin sensitisation theory dictates allergy arises from
- exposure through breaks in the skin
2. lack of GI exposure to the allergen.
type 1 hypersensitivity involves
IgE antibodies to a specific allergen trigger mast cells and basophils to release histamines and other cytokines. This causes an immediate reaction.
type 1 hypersensitivity reaction involves
range from itching, facial swelling and urticaria to anaphylaxis.
type 2 hypersensitivity reaction pathology
IgG and IgM antibodies react to an allergen and activate the complement system, leading to direct damage to the local cells.
examples of type 2 hypersensitivity reactions are
haemolytic disease of the newborn and transfusion reactions.
type 3 hypersensitivity reaction involves
Immune complexes accumulate and cause damage to local tissues.
type 3 hypersensitivity reaction examples
systemic lupus erythematosus (SLE), rheumatoid arthritis and Henoch-Schönlein purpura (HSP)
type 4 hypersensitivity reaction pathology
Cell mediated hypersensitivity reactions caused by T lymphocytes. T-cells are inappropriately activated, causing inflammation and damage to local tissues.
examples of type 4 hypersensitivity reactions include
organ transplant rejection and contact dermatitis.
three main ways to test for an allergy are
Skin prick testing
RAST testing, which involves blood tests for total and specific immunoglobulin E (IgE)
Food challenge testing
RAST testing involves
measures the total and allergen specific IgE quantities in the patient’s blood sample
following exposure to an allergen treatment is
Antihistamines (e.g. cetirizine)
Steroids (e.g. oral prednisolone, topical hydrocortisone or IV hydrocortisone)
Intramuscular adrenalin in anaphylaxis
symptoms of anaphylaxis are
Urticaria
Itching
Angio-oedema, with swelling around lips and eyes
Abdominal pain
anaphylaxis can be confirmed by
measuring the serum mast cell tryptase within 6 hours of the event
why most children be observed post anaphylactic episode?
as biphasic reactions can occur, meaning they can have a second anaphylactic reaction after successful treatment of the first.
tryptase is released upon
cell degranulation
examples of non sedating antihistamines are
cetirizine, loratadine and fexofenadine
examples of sedating histamines are
chlorphenamine (Piriton) and promethazine
rapid reaction to cows milk indicates what ab mediated cows milk allergy
IgE mediated.
is cows milk intolerance an allergic process?
no
GI symptoms of cows milk allergy?
Bloating and wind
Abdominal pain
Diarrhoea
Vomiting
general allergic symptoms to cows milk protein
Urticarial rash (hives) Angio-oedema (facial swelling) Cough or wheeze Sneezing Watery eyes Eczema
management of cow’s milk allergy is with
Breast feeding mothers should avoid dairy products
Replace formula with special hydrolysed formulas designed for cow’s milk allergy. every 6 months tried on the milk ladder.
what are signs of recurrent infection that should prompt referral?
Chronic diarrhoea since infancy
Failure to thrive
Appearing unusually well with quite a severe infection, for example afebrile with a large pneumonia
Significantly more infections than expected, particularly bacterial lower respiratory tract infections
Unusual or persistent infections such as cytomegalovirus, candida and pneumocystis jiroveci
tests for recurrent infections should include
FCB, immunoglobulins, complement proteins, antibody responses, HIV, CXR, sweat test and CT (bronchiectasis)
SCID presentation is
Persistent severe diarrhoea
Failure to thrive
Opportunistic infections that are more frequent or severe than in healthy children, for example severe and later fatal chickenpox, Pneumocystis jiroveci pneumonia and cytomegalovirus
Unwell after live vaccinations such as the BCG, MMR and nasal flu vaccine
Omenn syndrom
more than 50% of SCID cases are due to
mutations in the common gamma chain on the X chromosome that codes for interleukin receptors on T and B cells
omen syndrome is the result of a mutation on
t is the result of a mutation in the recombination-activating gene (RAG 1 or RAG 2) that codes for important proteins in T and B cells.
omen syndrome genetic transmission is through
autosomal recessive
features of omen syndrome are
A red, scaly, dry rash (erythroderma) Hair loss (alopecia) Diarrhoea Failure to thrive Lymphadenopathy Hepatosplenomegaly
Tx of SCID involves
Ig therapy, sterile enviroment, avoiding live vaccines, and haematopoietic stem cell transplantation
what infections are particularly common with B cell and immunoglobulin disorders
LRTI
the most common immunoglobulin deficiency is
IgA
IgA protects
mucous membranes, such as saliva, respiratory tract secretions, GI tract secretions, tears and sweat.
Common Variable Immunodeficiency results in deficiencies in
IgG and IgA, with or without a deficiency in IgM.
DiGeorge Syndrome is also known as
22q11.2 deletion syndrome,
22q11.2 deletion syndrome leads to what embryological birth defect?
developmental defect in the third pharyngeal pouch and third branchial cleft.
with 22q11.2 deletion syndrome and the developmental defect in the third pharyngeal pouch and third branchial cleft what is the clinical relevance of this?
One of the consequences of this is incomplete development of the thymus gland. An underdeveloped thymus gland results in an inability to create functional T cells.
features of digeorge syndrome are
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
Purine Nucleoside Phosphorylase Deficiency genetic transmission
autosomal recessive
Purine Nucleoside Phosphorylase Deficiency pathology
NPase is an enzyme that helps breakdown purines. Without this enzyme, a metabolite called dGTP builds up. This metabolite is exclusively toxic to T cells
result of Purine Nucleoside Phosphorylase Deficiency is
Clinically, patients immunity to infection gradually gets worse. They become increasingly susceptible to infections, particularly viruses and live vaccines.
Wiskott-Aldrich Syndrome genetic transmission is
X-linked
Wiskott-Aldrich Syndrome results in
abnormal functioning T cells
Ataxic Telangiectasia genetic transmission
autosomal recessive
Ataxic Telangiectasia effects the gene coding for
ATM serine/threonine kinase protein - important for DNA coding
Ataxic Telangiectasia gene defect is on chromosome
11
Ataxic Telangiectasia features
Low numbers of T-cells and immunoglobulins, causing immunodeficiency and recurrent infections.
Ataxia: problems with coordination due to cerebellar impairment
Telangiectasia, particularly in the sclera and damaged areas of skin
Predisposition to cancers, particularly haematological cancers
Slow growth and delayed puberty
Accelerated ageing
Liver failure
complement proteins are important for what organisms
Haemophilus influenza B
Streptococcus pneumonia
Neisseria meningitidis
complement deficiency and SLE pathology
as an incomplete complement cascade leads to immune complexes building up and being deposited in tissues, leading to chronic inflammation.
what complement deficiency is the most common?
C2
bradykinin role in inflammatory response
promoting blood vessel dilatation and increased vascular permeability, leading to angioedema
C1 esterase role is to
inhibit bradykinin
absence of C1 esterase leads too
intermittent angioedema in response to minor triggers, such as viral infections or stress, or without any clear trigger at all.
test for hereditary angioedema (C1 esterase inhibitor deficiency) is to check
he levels of C4 (compliment 4). C4 levels will be low in the condition
mannose-binding lectin leads to inhibition of the
alternative pathway of the complement system.
examples of inactivated vaccines
Polio
Flu vaccine
Hepatitis A
Rabies
examples of subunit and conjugate vaccines
Pneumococcus Meningococcus Hepatitis B Pertussis (whooping cough) Haemophilus influenza type B Human papillomavirus (HPV) Shingles (herpes-zoster virus)
examples 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
8 weeks vaccine schedule
6 in 1 vaccin
meningococcal type B
Rotavirus (oral vaccine)
6 in 1 vaccine covers
6 in 1 vaccine (diphtheria, tetanus, pertussis, polio, haemophilus influenzae type B (Hib) and hepatitis B)
12 weeks vaccine schedule
6 in 1 vaccine (again)
Pneumococcal (13 different serotypes)
Rotavirus (again
16 weeks vaccine schedule
6 in 1 vaccine (again)
Meningococcal type B (again)
1 year vaccine schedule
2 in 1 (haemophilus influenza type B and meningococcal type C) Pneumococcal (again) MMR vaccine (measles, mumps and rubella) Meningococcal type B (again)
3 years vaccine schedule
4 in 1 (diphtheria, tetanus, pertussis and polio) MMR vaccine (again)
12-13 years vaccine schedule
Human papillomavirus (HPV) vaccine (2 doses given 6 to 24 months apart)
14 years vaccine schedule
3 in 1 (tetanus, diphtheria and polio)
Meningococcal groups A, C, W and Y
sepsis pathology leading from recognition to immune activation
by macrophages, lymphocytes and mast cells. These cells release vast amounts of cytokines, to alert the immune system to the invader. These cytokines activate other parts of the immune system. This immune activation leads to further release of chemicals such as nitrous oxide The immune response causes inflammation throughout the body.
examples of cytokines
such as interleukins and tumor necrosis factor
nitrous oxide causes
that causes vasodilation.
role of cytokines in sepsis
cause the endothelial lining of blood vessels to become more permeable. This causes fluid to leak out of the blood into the extracellular space, leading to oedema and a reduction in intravascular volume.
consequences of oedema in sepsis
The oedema around blood vessels creates a space between the blood and the tissues, reducing the amount of oxygen that reaches the tissues.
activation of coagulation system in sepsis pathophysiology
coagulation system leads to deposition of fibrin throughout the circulation, further compromising organ and tissue perfusion. It also leads to consumption of platelets and clotting factors, as they are being used up to form the blood clots.
the consumption of platelets and clotting factors in sepsis leads too and is overall called
his leads to thrombocytopenia, haemorrhages and an inability to form clots and stop bleeding. This is called disseminated intravascular coagulopathy
the waste product of anaerobic respiration is
lactate
septic shock should be aggressively treated with
IV fluids
in ITU what drug is considered to aid in tissue perfusion during sepsis
inotropes (such as noradrenalin)
signs of sepsis
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)
any child under 3 months with a fever >38 need to be treated for
sepsis
immediate management for sepsis should involve
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 fluid bolus ratio for sepsis is
20ml/kg
when should an IV fluid bolus be delivered in sepsis
lactate >2mmol/L
Neisseria meningitidis is what sort of bacteria?
gram negative diploccous
Meningococcal septicaemia is the cause of the classic
non-blanching rash
non-blanching rash may be a sign of
disseminated intravascular coagulopathy (DIC) and subcutaneous haemorrhages
in neonates common cause of bacterial meningitis is
group B Streptococcus
neonate presentation of sepsis
hypotonia, poor feeding, lethargy, hypothermia and a bulging fontanelle.
lumbar puncture according to Nice should be a part of the investigations for
Under 1 months presenting with fever
1 to 3 months with fever and are unwell
Under 1 years with unexplained fever and other features of serious illness
two special tests for meningeal irritation are
Kernig’s test
Brudzinski’s test
kernig’s test involves
involves 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. This creates a slight stretch in the meninges.
positive kernig’s test will be when
there is meningitis it will produce spinal pain or resistance to movement.
bruzinski’s test involves
involves lying 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.
positive brudzinski’s test involves
In a positive test this causes the patient to involuntarily flex their hips and knees.
in community bacteria meningitis should involve
urgent stat injection (IM or IV) of benzylpenicillin prior to transfer to hospital as time is so important.
under 3 months antibiotics for meningitis should be
cefotaxime plus amoxicillin
older then 3 months antibiotics for meningitis should be
ceftriaxone
other considerations for meningitis treatment are
steroids dexamethasone for hearing loss and notify public health
post exposure prophylaxis to meningitis antibiotic is
single dose ciprofloxacin
bacteria in CSF
will release proteins and use up the glucose and stimulate neutrophils
viruses in CSF
don’t use glucose, release a small amount of protein and stimulate lymphocytes.
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
commonest cause of infective paediatric encephalitis is
herpes simplex virus
presentation of encephalitis
Altered consciousness Altered cognition Unusual behaviour Acute onset of focal neurological symptoms Acute onset of focal seizures Fever
diagnosis of encephalitis is with
lumbar puncture, viral PCR, CT, MRI, EEG, swabs and HIV
CI to lumbar punctures include
GCS below 9, haemodynamically unstable, active seizures or post-ictal.
herpes simplex virus (HSV) and varicella zoster virus (VZV) TX
aciclovir
CMV Tx
Ganciclovir
infective mononucleosis is caused by
epstein barr virus
infective mononucelosis is also known as
glandular fever
adolescent with a sore throat, who develops an itchy rash after taking amoxicillin what is the underlyign cause?
infective mononucleosis
features of infective mononucelosis
Fever Sore throat Fatigue Lymphadenopathy (swollen lymph nodes) Tonsillar enlargement Splenomegaly and in rare cases splenic rupture
in infectious mononucleosis the body produces
heterophile antibodies
heterophile antibodies can be tested for via
Monospot test: this introduces the patient’s blood to red blood cells from horses or Paul-Bunnell test: this is similar to the monospot test but uses red blood cells from sheep.
acute infection by EBV would be demonstrated through
IgM
immunity to EBV would be demonstrated by
IgG
EBV is associated with
buritt’s lymphoma
mumps is a what infection and spread by?
viral infection spread by respiratory droplets
presentation of mumps is
initial period of flu-like symptoms known as the prodrome. These occur a few days before the parotid swelling:
Fever Muscle aches Lethargy Reduced appetite Headache Dry mouth
complications of mumps presentation
Abdominal pain (pancreatitis)
Testicular pain and swelling (orchitis)
Confusion, neck stiffness and headache (meningitis or encephalitis)
mumps Dx
PCR testing on a sliva swab
who must you notify with a mumps infection?
public health
how may HIV spread to a child?
pregnancy, birth or breastfeeding. This is referred to as vertical transmission.
prophylaxis for HIV during birth if >10000 copies/ml
IV zidovudine
hepatitis B is what sort of virus?
DNA
spread of hepatitis B is
vertical, or blood, or sex.
infection history for hep B
Most children fully recover from the infection within 2 months, however a portion go on to become chronic hepatitis B carriers.
Surface antigen (HBsAg) indicates
active infection
E antigen (HBeAg) indicates
marker of viral replication and implies high infectivity
Core antibodies (HBcAb) indicates
implies past or current infection
Surface antibody (HBsAb) indicates
implies vaccination or past or current infection
Hepatitis B virus DNA (HBV DNA) is used for
this is a direct count of the viral load
initial viral markers for hep B should be
HBcAb (for previous infection) and HBsAg (for active infection)
levels of HBeAG reflect
infectivity
Hep B + mothers within 24 hours of birth should be given
Hepatitis B vaccine
Hepatitis B immunoglobulin infusion
is it safe for hep B breastfeeding?
yes if received vaccine and immunoglobulin infusion.
hep C type of virus
RNA virus
disease course of Hep C in adults
1 in 4 fight off the virus and make a full recovery
3 in 4 develop chronic hepatitis C
complications of Hep c in adults
Liver cirrhosis and associated complications of cirrhosis
Hepatocellular carcinoma
testing for Hep C involves
Hepatitis C antibody is the screening test
Hepatitis C RNA testing
Hepatitis C RNA testing is used to
confirm the diagnosis of hepatitis C, calculate viral load and identify the genotype
does Hep C spread via breastfeeding?
no
in children over 3 years old treatment for hep C inovles
pegylated interferon and ribavirin, but treatment is usually delayed until adulthood
commonest cause of bacterial tonsillitis is
group A streptococcus (Streptococcus pyogenes)
most common cause of otitis media, rhino sinusitis and second most common bacterial cause of tonsillitis is
Streptococcus pneumoniae.
waldeyer’s tonsillar ring refers too
adenoid, tubal tonsils, palatine tonsils and the lingual tonsil.
centor criteria is for
probability of tonsillitis being due to bacteria infection
centor criteria are
Fever over 38ºC
Tonsillar exudates
Absence of cough
Tender anterior cervical lymph nodes (lymphadenopathy)
alternative to the centor critera is the
FeverPAIN score
feverpain criteria
Fever during previous 24 hours P – Purulence (pus on tonsils) A – Attended within 3 days of the onset of symptoms I – Inflamed tonsils (severely inflamed) N – No cough or coryza
first line for antibiotics in tonsillitis
penicillin.
quinsy refers too and is a complication of
peritonsillar abscess, tonsillitis
presentation of quinsy
Sore throat Painful swallowing Fever Neck pain Referred ear pain Swollen tender lymph nodes Trismus (unable to open mouth) changes in voice.
Tx for quinsy is
incision and drainage under GA
No of episodes required for tonsillectomy
7 or more in 1 year
5 per year for 2 years
3 per year for 3 year
complication of tonsillectomy is
bleeding
options for post tonsillectomy bleeding are
IV access, group and save/crossmatch, hydrogen peroxide gargles or adrenalin topically applied.
Otitis media is the name given to the
infection of the middle ear
presentation of otitis media is
ear pain, reduced hearing, fever, cough, coryzal symptoms, sore throat and general unwellness
normal tympanic membrane should look like
“pearly-grey”, translucent and slightly shiny. with cone of light reflex.
otitis media ear presentation
bulging, red, inflamed looking membrane.
for severe otitis media or immunocompromised antibiotics should be
amoxicillin for 5 days
glue ear is known as
otitis media with effusion.
otoscopy of glue ear should reveal
dull tympanic membrane with air bubbles of visible fluid level.
if necessary glue ear may be treated with
grommets.
audiometry sensorineural hearing loss results
both air and bone conduction readings will be more than 20 dB, plotted below the 20 dB line on the chart. on affected sides
conductive hearing loss, audiometry results
bone conduction readings will be normal (between 0 and 20 dB), however air conduction readings will be greater than 20 dB,
mixed hearing loss audiometry results
both air and bone conduction readings will be more than 20 dB, however there will be a difference of more than 15 dB between the two (bone conduction > air conduction).
nosebleeds commonly arise from
Kiesselbach’s plexus, which is also known as Little’s area
unstable severe nosebleed may require
Nasal packing using nasal tampons or inflatable packs
Nasal cautery using a silver nitrate stick
cystic hygroma is a malformation of the
lymphatic system
cystic hygroma can often me found on the
posterior triangle of the neck left side
features of cystic hygromas are
Can be very large
Are soft
Are non-tender
Transilluminate
mx of cystic hygroma is
aspiration
thyroglossal cyst is the result of what persisting?
thyroglossal duct
differential for thyroglossal cyst is
ectopic thyroid tissue
features of thyroglossal cysts is
Mobile
Non-tender
Soft
Fluctuant
diagnosis of thyroglossal cyst is
US or CT
branchial cyst is the result of
second branchial cleft fails to properly form and instead the space fills with fluid
branchial cyst usually presents
round, soft, cystic swelling between the angle of the jaw and the sternocleidomastoid muscle in the anterior triangle of the neck. This swelling will transilluminate with light,
growth plates are made from
hyaline cartilage
growth plate sits between the
epiphysis and metaphysis
children have more what type of bone compared to adults
cancellous, flexible but less strong compared to cortical in adults.
most likely fracture for children
greenstick, one side of the bone breaks.
growth plate fractures classification are called
Salter Harris classification
Salter harris classification of fractures
Type 1: Straight across Type 2: Above Type 3: BeLow Type 4: Through Type 5: CRush
first principle of managing a fracture
mechanical alignment
Closed reduction via manipulation of the joint
Open reduction via surgery
second principle of managing a fracture
achieving relative stability via
External casts K wires Intramedullary wires Intramedullary nails Screws Plate and screws
pain management in children step 1 and step 2
Step 1: Paracetamol or ibuprofen
Step 2: Morphine
why is aspirin CI in children
spirin is contraindicated in children under 16 due to the risk of Reye’s syndrome
0-4 years differentials for hip pain
Septic arthritis
Developmental dysplasia of the hip (DDH)
Transient sinovitis
5-10 years differentials for hip pain
Septic arthritis
Transient sinovitis
Perthes disease
10-16 years differentials for hip pain
Septic arthritis
Slipped upper femoral epiphysis (SUFE)
Juvenile idiopathic arthritis
red flags for hip pain are
Child under 3 years Fever Waking at night with pain Weight loss Anorexia Night sweats Fatigue Persistent pain Stiffness in the morning Swollen or red joint
presentation of septic arthritis
Hot, red, swollen and painful joint
Refusing to weight bear
Stiffness and reduced range of motion
Systemic symptoms such as fever, lethargy and sepsis
commonest cause of septic arthritis
staph. aureus
other bacteria involved in septic arthritis
Neisseria gonorrhoea (gonococcus) in sexually active teenagers
Group A streptococcus (Streptococcus pyogenes)
Haemophilus influenza
Escherichia coli (E. coli)
Ix of septic arthritis includes
aspiration with gram staining, crystal microscopy, culture and antibiotics sensitivities
does transient synovitis occur alongside a fever?
no
transient synovitis often occurs a few weeks post
viral URTI
pathology of Perthe’s disease is
Perthes disease involves disruption of blood flow to the femoral head, causing avascular necrosis of the bone
main complication of Perther’s disease is
neovascularisation leading to a soft and deformed femoral head causing early osteoarthritis
Perthe’s presentation
Perthes disease present with a slow onset of:
Pain in the hip or groin
Limp
Restricted hip movements
There may be referred pain to the knee
NO HISTORY OF TRAUMA
Ix for Perthe’s disease
X-rat first lne, blood tests, technetium bone scan and MRI
Mx of perthe’s involves
regular x-rays, Bed rest Traction Crutches Analgesia PT and sometimes surgery.
SUFE refers too
slipped capital femoral epiphysis
presenting symptoms of SUFE
Hip, groin, thigh or knee pain
Restricted range of hip movement
Painful limp
Restricted movement in the hip
examination signs of SUFE
hip will be externally rotated and restricted internal rotation
common bacteria for osteomyelitis is
Staph. aureus
presentation of osteomyelitis
Refusing to use the limb or weight bear Pain Swelling Tenderness low grade fever
IX for osteomyelitis
x-rays, MRI, bone scan, blood tests (WBC, ESR, CRP), blood culture, bone marrow aspirate or bone biopsy,
mx for osteomyelitis
antibiotics therapy, drainage and debridement.
common site for osteosarcoma is the
femur
main presenting features for osteosarcoma are
persistent bone pain, bone swelling, a palpable mass and restricted joint movements.
Dx for osteosarcoma is
urgent X-ray, raised ALK P,
staging for osteosarcoma involves
CT scan MRI scan Bone scan PET scan Bone biopsy
X-ray of osteosarcoma will reveal
periosteal reaction (irritation of the lining of the bone) that is classically described as a “sun-burst” appearance
Mx of osteosarcoma is
MDT, surgical resection, limp amputation and adjuvant chemotherapy.
talipes equinovarus refers too
plantar flexion and supination.
Talipes calcaneovalgus refers too
dorsiflexion and pronation.
non-surgical method for treating talipes is
Ponseti method - cast is applied to hold it in position. This is repeated over and over until the foot is in the correct position.
Developmental dysplasia of the hip (DDH) refers too
abnormal development leading to instability in the hips and a tendency or potential for subluxation or dislocation.
Risk factors for DDH
First degree family history
Breech presentation from 36 weeks onwards
Breech presentation at birth if 28 weeks onwards
Multiple pregnancy
examination signs that indicate DDH are
Different leg lengths
Restricted hip abduction on one side
Significant bilateral restriction in abduction
Difference in the knee level when the hips are flexed
Clunking of the hips on special tests
two tests for DDH are
ortolani test and barlow test
ortolani test involves
with the baby on their back with the hips and knees flexed, abduct the hips and apply pressure to anteriorly dislocate hips.
barlow test invovles
baby on their back with the hips adducted and flexed at 90 degrees and knees bent at 90 degrees to see if femoral head will dislocate posteriorly
suspicion of DDH warrants
US
Mx of DDH is through
palvik harness to keep the hips flexed and abducted. surgical requires a hip spica cast to immobilise the hip.
ricket’s is caused by
deficiency in vitamin D or calcium
vit D is essential for
essential in calcium and phosphate absorption from the intestines and kidneys as well as regulating bone turnover and reabsorption.
low calcium causes
secondary hyperparathyroidism as the parathyroid gland tries to raise the calcium level by secreting parathyroid hormone.
rickets/osteomalacia presents with
Lethargy Bone pain Swollen wrists Bone deformity Poor growth Dental problems Muscle weakness Pathological or abnormal fractures
ricket bone deformities include
bowing of the legs, knock knees, craniotabes (soft skull), delayed teeth development, rachitic rosary where the ends of the rips expand.
initial Ix for rickets are
Serum 25-hydroxyvitamin D and X-ray
other Ix for rickett’s
Serum calcium may be low
Serum phosphate may be low
Serum alkaline phosphatase may be high
Parathyroid hormone may be high
Tx of ricket’s
Vit D replacement and calcium supplementation.
achondroplasia is the common cause of
disproportionate short stature
achondroplasia gene is the
fibroblast growth factor receptor 3 (FGFR3), is on chromosome 4.
genetic transmission of achondroplasia is
autosomal dominant
Osgood-Schlatters Disease is caused by
inflammation at the tibial tuberosity where the patella ligament inserts.
typical demographic for presentation of osgood schlatters disease
It typically occurs in patients aged 10 – 15 years, and is more common in males. Osgood-Schlatter disease is usually unilateral, but it can be bilateral.
presentation of osgood schlatter’s disease
Visible or palpable hard and tender lump at the tibial tuberosity
Pain in the anterior aspect of the knee
The pain is exacerbated by physical activity, kneeling and on extension of the knee
Mx of osgood schlatter’s disease
Reduction in physical activity
Ice
NSAIDS (ibuprofen) for symptomatic relief
stretching and PT post
rare complication of osgood schlatter’s disease is
avulsion fracture
osteogenesis imperfecta is also known as
brittle boen disease
pathology of osteogenesis imperfecta is
collegen malformation
presentation of osteogenesis imperfecta
Hypermobility
Blue / grey sclera (the “whites” of the eyes)
Triangular face
Short stature
Deafness from early adulthood
Dental problems, particularly with formation of teeth
Bone deformities, such as bowed legs and scoliosis
Joint and bone pain
medical treatments for osteogensis imperfecta are
Bisphosphates to increase bone density
Vitamin D supplementation to prevent deficiency
acute rheumatic fever is triggered by
autoimmune condition triggered by streptococcus bacteria.
pathophysiology of rheumatic fever
group A beta-haemolytic streptococcal stimulate ab response but the antigens matches that of the myocardium of the heart.
rheumatic fever is an example of what type of hypersensitivity reaction.
type 2
presentation of rheumatic fever
2-4 weeks following tonsillitis with: Fever Joint pain Rash Shortness of breath Chorea Nodules
and migratory arthritis
heart involvement of rheumatic fever
Tachycardia or bradycardia
Murmurs from valvular heart disease, typically mitral valve disease
Pericardial rub on auscultation
Heart failur
skin involvement of rheumatic fever includes
Firm painless nodules occur over extensor surfaces of joints, such as the elbows. The erythema marginatum rash involves pink rings of varying sizes affecting the torso and proximal limbs.
CNS involvement of rheumatic fever includes
this involves irregular, uncontrolled and rapid movements of the limbs. known as chorea or St vitus’ dance
assessment for rheumatic fever includes
Throat swab for bacterial culture
ASO antibody titres
Echocardiogram, ECG and chest xray
criteria for diagnosis of rheumatic feveris
Jones criteria
major Jones crtieria for rheumatic fever
two of J – Joint arthritis O – Organ inflammation, such as carditis N – Nodules E – Erythema marginatum rash S – Sydenham chorea
minor criteria for rheumatic fever are
Fever
ECG Changes (prolonged PR interval) without carditis
Arthralgia without arthritis
Raised inflammatory markers (CRP and ESR)
management of rheumatic fever should invovle
NSAIDs (e.g. ibuprofen) are helpful for treating joint pain
Aspirin and steroids are used to treat carditis
Prophylactic antibiotics (oral or intramuscular penicillin) are used to prevent further streptococcal infections and recurrence of the rheumatic fever. These are continued into adulthood.
Monitoring and management of complications
kawasaki disease is an example of
medium vessel vasculitis
features of kawasaki disease are
ersistent high fever (above 39ºC) for more than 5 days. Children will be unhappy and unwell. The key skin findings are a widespread erythematous maculopapular rash and desquamation
plus: Strawberry tongue (red tongue with large papillae) Cracked lips Cervical lymphadenopathy Bilateral conjunctivitis
ix for Kawasaki disease include
Full blood count can show anaemia, leukocytosis and thrombocytosis
Liver function tests can show hypoalbuminemia and elevated liver enzymes
Inflammatory markers (particularly ESR) are raised
Urinalysis can show raised white blood cells without infection
Echocardiogram can demonstrate coronary artery pathology
Tx for kawaski disease includes
High dose aspirin to reduce the risk of thrombosis
IV immunoglobulins to reduce the risk of coronary artery aneurysms
Henoch-Scholein purpura is an example of
IgA vasculitis with a purpuric rash.
presentation of HSP
Purpura (100%), Joint pain (75%), Abdominal pain (50%) Renal involvement (50%)
risk of HSP complications with abdominal pain
gastrointestinal haemorrhage, intussusception and bowel infarction.
HSP effect on the kidneys are
IgA nephritis with risk of nephrotic syndrome.
Mx of HSP is with
supportive with urine dipstick monitoring and blood pressure monitoring.
ehler’s danlos syndrome is an example of
enetic conditions that cause defects in collagen, resulting in hypermobility of the patient’s joints and abnormalities in connective tissue
presentation of ehlers danlos syndrome is
Hypermobility in joints Joint pain after exercise or inactivity Joint dislocations, for example the shoulders or hips Soft stretchy skin Easy bruising Poor healing of wounds Bleeding Headaches Autonomic dysfunction causing dizziness and syncope Gastro-oesophageal reflux Abdominal pain Irritable bowel syndrome Menorrhagia and dysmenorrhea Premature rupture of membranes in pregnancy Urinary incontinence Pelvic organ prolapse Temporomandibular joint dysfunction Myopia and othe
what is the score system for hypermobility
Beighton
beighton score for hypermobility
Palms flat on floor with straight legs (score 1)
Elbows hyperextend
Knees hyperextend
Thumb can bend to touch the forearm
Little finger hyperextends past 90 degrees
what syndrome can occur alongside ehler danlos syndrome
Postural orthostatic tachycardia, result of autonomic dysfunction resulting in presyncope, syncope
systemic JIA is also known as
Still’s disease
systemic JIA (still’s disease) presents with
Subtle salmon-pink rash High swinging fevers Enlarged lymph nodes Weight loss Joint inflammation and pain Splenomegaly Muscle pain Pleuritis and pericarditis
biochemical markers of systemic JIA are
Antinuclear antibodies and rheumatoid factors are typically negative. There will be raised inflammatory markers, with raised CRP, ESR, platelets and serum ferritin.
key complication of JIA is
macrophage activation syndrome (MAS),
macrophage activation syndrome (MAS) involves
It presents with an acutely unwell child with disseminated intravascular coagulation (DIC), anaemia, thrombocytopenia, bleeding and a non-blanching rash. It is life threatening. A key investigation finding is a low ESR.
In children that have fevers for more than 5 days, the key non-infective differentials to remember
are Kawasaki disease, Still’s disease, rheumatic fever and leukaemia.
Polyarticular JIA is the equivalent of
rheumatoid arthritis: most kids are seronegative for rheumatoid factor.
polyarticular JIA presents with
mild fever, anaemia and reduced growth.
Oligoarticular JIA classic associated feature is
A classic associated feature with oligoarticular JIA is anterior uveitis. Patients should be referred to an ophthalmologist for management and follow up of uveitis.
Oligoarticular JIA commonly effects the
larger joints such as the knee or ankle.
Oligoarticular JIA biochem
Antinuclear antibodies are often positive, however rheumatoid factor is usually negative.
The majority of patients with enthesitis-related arthritis have the what gene?
HLA B27 gene.
entheses refers too
tendon of a muscle inserts into a bone.
When assessing patients for enthesitis-related arthritis, consider signs and symptoms of
psoriasis (psoriatic plaques and nail pitting) and inflammatory bowel disease (intermitted diarrhoea and rectal bleeding).
enthesitis-related arthritis are prone too
prone to anterior uveitis, and should see an ophthalmologist for screening, even if they are asymptomatic.
psoriatic arthritis is a
seronegative inflammatory arthritis associated with psoriasis, with either polyarthritis affecting small joints or asymmetrical arthritis affecting large joints of the lower limb
medical Mx of JIA
NSAIDs, such as ibuprofen
Steroids
Disease modifying anti-rheumatic drugs (DMARDs)
Biologic therapy, such as the tumour necrosis factor inhibitors
Disease modifying anti-rheumatic drugs (DMARDs) examples
such as methotrexate, sulfasalazine and leflunomide
TNF inhibitor examples
etanercept, infliximab and adalimumab
eczema presents usually with
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.
pathophysiology of eczema
eczema is caused by defects in the barrier that the skin provides. Tiny gaps in the skin barrier provide an entrance for irritants, microbes and allergens that create an immune response,
the key to maintenance of eczema is
create an artificial barrier over the skin to compensate for the defective skin barrier. this is via thick greasy emollients.
specialist treatments for eczema include
severe eczema include zinc impregnated bandages, topical tacrolimus, phototherapy and systemic immunosuppressants, such as oral corticosteroids, methotrexate and azathioprine.
steroid ladder mild
Mild: Hydrocortisone 0.5%, 1% and 2.5%
very potent steroid ladder
Dermovate (clobetasol propionate 0.05%)
complications of topical steroid application for eczema
thinning of the skin, stretch marks, bruising and telangiectasia.
commonest opportunistic infection in eczema is
staphylococcus aureus
eczema herperticum is a viral skin infection caused by
commonly herpes simplex virus (HSV) or varicella zoster virus (VZV)
presentation of eczema herpeticum is
widespread, painful, vesicular rash with systemic symptoms such as fever, lethargy, irritability and reduced oral intake. There will usually be lymphadenopathy (swollen lymph nodes).
management of eczema herpeticum is with
aciclovir.
presentattion of psoriasis
dry, flaky, scaly, faintly erythematous skin lesions that appear in raised and rough plaques, commonly over the extensor surfaces of the elbows and knees and on the scalp
guttate psoriasis presents as
commonly occurs in children. It presents with many small raised papules across the trunk and limbs. The papules are mildly erythematous and can be slightly scaly.
guttate psoriasis can be triggered by
streptococcal throat infection
what are the two types of psoriasis that are considered emergencies?
Pustular psoriasis and Erythrodermic psoriasis
three signs of psoriasis
auspitz sign, koebner phenomenon, residual pigmentation.
auspitz sign refers too
small points of bleeding when plaques are scraped off
koebner phenomenon refers too
development of psoriatic lesions to areas of skin affected by trauma
management of psoriasis is through
Topical steroids
Topical vitamin D analogues (calcipotriol)
Topical dithranol
Topical calcineurin inhibitors (tacrolimus) are usually only used in adults
Phototherapy with narrow band ultraviolet B light is particularly useful in extensive guttate psoriasis
specialist treatment of psoriasis includes
this might include methotrexate, cyclosporine, retinoids or biologic medications.
psoriasis nail signs include
nail pitting, thickening, discolouration, ridging and onycholysis (separation of the nail from the nail bed).
psoriasis is associated with
obesity, hyperlipidaemia, hypertension and type 2 diabetes.
what bacteria plays a key role in acne?
Propionibacterium acnes
pathology of acne.
increased sebum trapping kerating and blocking the pilosebaceous unit. this leads to swelling and inflammation as the follicle becomes infected.
Macules are
flat marks on the skin
papules are
small lumps on the skin
management to reduce inflammation in acne is
Topical benzoyl peroxide reduces inflammation, helps unblock the skin and is toxic to the P. acnes bacteria
what treatments reduce production of sebum in acne
topical retinoids (chemicals related to vitamin A) slow the production of sebum or Oral contraceptive pill can help female patients stabilise their hormones and slow the production of sebum
antibiotic options for acne are
Topical antibiotics such as clindamycin (prescribed with benzoyl peroxide to reduce bacterial resistance)
Oral antibiotics such as lymecycline
last line option for acne includes
Oral retinoids for severe acne (i.e. isotretinoin)
complications of isotretinoin.
Dry skin and lips
Photosensitivity of the skin to sunlight
Depression, anxiety, aggression and suicidal ideation. Patients should be screened for mental health issues prior to starting treatment.
Rarely Stevens-Johnson syndrome and toxic epidermal necrolysis
teratogenic.
measles rash appears as
Koplik spots are greyish white spots on the buccal mucosa. They appear 2 days after the fever. They are pathognomonic
natural history for measles rash is
The rash starts on the face, classically behind the ears, 3 – 5 days after the fever. It then spreads to the rest of the body. The rash is an erythematous, macular rash with flat lesions.
scarlet fever rash usually appears as
red-pink, blotchy, macular rash with rough “sandpaper” skin that starts on the trunk and spreads outwards. Patients can have red, flushed cheeks.
Tx for scarlet fever is
phenoxymethylpenicillin (penicillin V) for 10 days
features of scarlet fever are
Fever Lethargy Flushed face Sore throat Strawberry tongue Cervical lymphadenopathy
cause of scarlet fever is
streptococcus pyogenes (group A strep) bacteria.
is scarlet fever a notifiable disease?
yes notify public health.
rubella rash is
milder erythematous macular rash compared with measles. The rash starts on the face and spreads to the rest of the body.
rubella lash usually lasts
The rash classically lasts 3 days.
Parvovirus causes what kind of rash?
fifth disease, slapped cheek syndrome and erythema infectiosum.
parvovirus infection 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”. A few days later a reticular mildly erythematous rash affecting the trunk and limbs appears that can be raised and itchy. Reticular means net-like
Roseola Infantum is caused by
human herpesvirus 6 (HHV-6)
presentation of roseola infantum
It presents 1 – 2 weeks after infection with a high fever (up to 40ºC) that comes on suddenly, lasts for 3 – 5 days and then disappears suddenly. There may be coryzal symptoms, sore throat and swollen lymph nodes during the illness. When the fever settles, the rash appears for 1 – 2 days. The rash consists of a mild erythematous macular rash across the arms, legs, trunk and face and is not itchy.
key complication of roseola infantum
febrile convulsion.
erythema multiform presents with
produces characteristic “target lesions”. Target lesions are red rings within larger red rings, with the darkest red at the centre, similar to a bulls-eye target. It does not usually affect the mucous membranes but can cause a sore mouth (stomatitis). as well as flu like symptoms.
erythema multiform is a rash caused by
hypersensitivity reaction.
erythema multiform with no underlying cause should prompt suspicion of
mycoplasma pneumonia.
urticaria caused by the release of
histamine
urticaria Mx is
Fexofenadine is usually the antihistamine of choice for chronic urticaria. Oral steroids may be considered as a short course for severe flares.
specialist options for urticaria
Anti-leukotrienes such as montelukast
Omalizumab, which targets IgE
Cyclosporin
chickenpox rash is
widespread, erythematous, raised, vesicular (fluid filled), blistering lesions. The rash usually starts on the trunk or face and spreads outwards affecting the whole body over 2 – 5 days. Eventually the lesions scab over, at which point they stop being contagious.
chickenpox is caused by and spread through
Varicella zoster virus and spread spread through direct contact with the lesions or through infected droplets from a cough or sneeze.
VZV lays dormant in the
sensory dorsal root ganglion cells and cranial nerves reactivate later in life as shingles or Ramsay Hunt syndrome.
chickenpox itching can be eased with
calamine lotion and chlorphenamine (antihistamine).
hand, foot and mouth disease may be managed by
coxsackie A virus
hand, foot and mouth disease presentation
ypical viral upper respiratory tract symptoms such as tiredness, sore throat, dry cough and raised temperature. After 1 – 2 days small mouth ulcers appear, followed by blistering red spots across the body.
Molluscum Contagiosum is caused by
pox virus
Molluscum Contagiosum presentation
small, flesh coloured papules (raised individual bumps on the skin) that characteristically have a central dimple.
Pityriasis Rosea prodrome
These include headache, tiredness, loss of appetite and flu-like symptoms.
Pityriasis Rosea initial rash
herald patch. This is a faint red or pink, scaly, oval shaped lesion that is 2cm or more in diameter, usually occurring somewhere on the torso.
Pityriasis Rosea later rash general presentation
The rash consists of widespread faint red or pink, slightly scaly, oval shaped lesions, usually less than 2 cm in diameter. On the torso they can be arranged in a characteristic “christmas tree” fashion,
Seborrhoeic Dermatitis effects the
scalp, nasolabial folds and eyebrows.
Seborrhoeic Dermatitis cause
malassezia yeast
first line treatment for infantile seborrheoic dermatitis
First line treatment is by applying baby oil, vegetable oil or olive oil, gently brushing the scalp then washing off. When this is not effective, white petroleum jelly can be used overnight to soften the crusted areas before washing off in the morning.
second line for infantile seborrhoeic dermatitis
clotrimazole or miconazole
first line for paediatric seborrhoeic dermatitis of the scalp
ketoconazole shampoo
tinea capitis refers too
refers to ringworm affecting the scalp
Tinea pedis refers to
ringworm affecting the feet, also known as athletes foot
tinea cruris refers too
ringworm of the groin
tinea corporis refers too
ringworm of the body
onychomycosis refers too
fungal nail infection
most common type of fungus to cause ringworm is called
trichophyton
ring worm presents as
itchy rash that is erythematous, scaly and well demarcated. There is often one or several rings or circular shaped areas that spread outwards, with a well demarcated edge. The edge is more prominent and red and the area in the centre is more faint in colour.
Mx of ringworm is with
icroscopy, culture and anti-fungals
antifungal creams include
clotrimazole and miconazole
oral antifungals include
fluconazole, griseofulvin and itraconazole
tinea incognito may be caused by
treating ringworm with steroids.
scabies are caused by
Sarcoptes scabiei
scabies presents with
incredibly itchy small red spots, possibly with track marks where the mites have burrowed. The classic location of the rash is between the finger webs,
scabies are treated with
permethrin cream over whole body, or Oral ivermectin as a single dose
scabies in the immunocomprimised may cause
crusted scabies.
erythema nodosum pathology
hypersensitivity reaction causing inflammation of subcutaneous fat on the shins.
erythema nodosum often indicates
IBD or sarcoidosis
impetigo usually presents as
golden crust
impetigo often caused by
staphylococcus skin infection
Tx for non bullous impetigo includes
Topical fusidic acid , antiseptic cream or in severe cases oral flucloxacillin.
widespread bullous impetigo is called
staphylococcus scalded skin syndrome.
staphylococcus scalded skin syndrome pathology
Staph. aureus produced epidermolytic toxins that are protease enzymes
what sign is positive in SSSS syndrome
nikolsky sign
nikolsky sign refers too
ery gentle rubbing of the skin causes it to peel away.
Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) refer too
epidermal necrosis, resulting in blistering and shedding of the top layer of skin.
Tx for SJS and toxic epidermal necrolysis are
steroids, immunoglobulins and immunosuppressant medications
