General Flashcards
Coeliac
sx, ix, mx
Background
Can start as early as weaning, when infants first exposed to gluten.
Signs and symptoms
Similar to adults (altered stool, anaemia), plus some more specific features:
Constipation and/or diarrhoea.
Poor growth, ↓stature.
Irritable
Wasted buttocks.
Abdominal protrusion.
↑RR.
Obesity
def, causes, Ix, comp
Definitions
Obesity: BMI >98th centile
Overweight: BMI >91st centile.
Causes
Nearly always due to lifestyle.
Very rarely due to underlying disease such as hypothyroidism, Cushing’s, or Prader Willi. Often accompanied by short stature.
Investigations
No shoes and light clothing for measuring height and weight.
Complications
Hypertension
Endocrine: type 2 diabetes, PCOS.
Orthopaedic problems.
Idiopathic intracranial hypertension.
Asthma
Depression
Short stature
def, causes, ix
Definition
Height <2nd centile.
Causes
Familial short stature (80%) i.e. small parents. Predicted height can be calculated in a gender-specific formula using mid-parental height.
Constitutional delay in growth and puberty. Benign and needs no investigation. Bone age is matched with height age (with both below average for chronological age), differentiating it from serious pathology where bone age is severely delayed.
IUGR
Psychosocial: neglect, poverty.
Genetic: Down’s, Turner’s, CF, dwarfism.
GI: Coeliac, IBD.
Endocrine: steroid treatments, hypothyroidism, growth hormone deficiency.
Investigations:
Baseline bloods
- FBC, U&Es, LFTs, bone profile, TFTs, CRP, ESR
Specialist bloods
- Anti-TTG, growth hormone provocation tests, 9 AM cortisol and dexamethasone suppression test
Genetics
- karyotyping
Imaging
- Xray of L hand and wrist (bone age)
- MRI (if neuro signs/sypresent)
- Limited skeletalsurvery(scoliosis, skeletal dysplasia)
Influenza
path, Epi, sx, dx, mx, comp
Pathophysiology
Influenza A and B are RNA viruses of the Orthomyxoviridae family. A and B vary in matrix proteins and nucleoproteins. Their surface glycoproteins include hemagglutinin and neuraminidase, the types of which are used to classify influenza A strains.
Influenza A is more common, severe, and causes epi/pandemics like H5N1 (aVIan) and H1N1 (swINe). Influenza B is milder and, unlike A, occurs almost exclusively in humans.
Spread through droplets, so masks help prevent transmission.
1-3 days incubation.
Epidemiology
Incidence peaks in colder months, ‘flu season’. Possible reasons for this are increased indoor human contact due to the weather, cold and humidity aiding viral survival, and low vitamin D levels leading to impaired immune function.
20% of the population are infected each flu season. Most remain asymptomatic carriers, with only 1 in 4 (5% of the population) becoming symptomatic, usually with mild upper respiratory tract symptoms. Only 1 in 5 symptomatic individuals (1% of the population) present to a doctor, and even then it is often not recognized as flu. As with many infectious outbreaks, we only see the tip of the iceberg.
Presentation
Quick onset.
Respiratory symptoms: cough, coryza.
Systemic symptoms: fever, rigors, fatigue, anorexia.
Pain: headache, myalgia.
Other symptoms: nausea and vomiting, conjunctivitis, photophobia.
Diagnosis
Usually a clinical diagnosis, but nasal/throat swabs for viral culture or PCR are useful for confirmation in severe disease and for epidemiological surveillance.
Management
Prevention:
Vaccination reduces infection, symptomatic disease, and complications by around 50%.
Route: whole trivalent vaccine IM, or fragmented nasal vaccine if <13 years old.
Indications: toddlers, age >65, diabetes, respiratory disease (COPD, asthma), organ failure (heart, liver, kidney), immunosuppressed.
Treatment:
Rest, paracetamol, and hydration.
Neuraminidase inhibitors can be given if over 1 years old and it is within the first 48 hours of symptoms. May reduce symptom duration by 1 day, but evidence on reducing complications is unclear. Oseltamivir (oral) can cause nausea and vomiting, and zanamivir (nasal) can cause bronchospasm so is avoided in asthma and COPD.
Complications
Pneumonia can result directly from influenza itself or, more commonly, secondary bacterial infection (Strep. pneumo, Staph. aureus, H. influenzae). Implicated in many influenza deaths.
Other local infections: bronchitis, sinusitis, otitis media.
Neurological complications: encephalitis, post-influenza encephalopathy in children, Guillain-Barré syndrome.
Kawasaki
def, sx, mx
Definition and epidemiology
Medium vessel vasculitis.
Commonest around age 2, and rare after 5.
Signs and symptoms
Persistent fever, >5 days.
Dry, bilateral conjunctivitis.
Non-vesicular, desquamating rash, which starts at the extremities (inc. palms and soles).
Strawberry tongue.
Management
Acute: aspirin and IVIG (IV immunoglobulin). The one time where aspirin is used in kids, despite the risks of Reye’s.
Long-term: lifelong aspirin as 25% develop coronary artery aneurysms and are at risk of early MI.
Otitis media
path, rf, sx, mx, comp
Pathophysiology
Middle ear inflammation.
Pathogens: Strep. pneumo, nontypeable H. influenzae, Moraxella.
75% occur <10 years old, especially 6-18 months.
Risk factors
Smoking
URTI
Bottle-feeding and dummy use.
Adenoids
Anatomical malformations.
Signs and symptoms
Acute otitis media:
Sudden pain and fever.
Inflammed, bulging ear drum, or purulent discharge and resolution of pain if it has burst.
May follow URTI.
Other possible symptoms: irritability, anorexia, and vomiting.
Chronic otitis media:
Several months of symptoms.
Fluid discharge.
Management
Usually self-resolves within 3 days, but can last up to 1 week.
Consider amoxicillin for 5 days if: perforated tympanic membrane (and/or discharge in ear canal), ≥4 days symptoms, or bilateral OM <2 years old.
Complications
Glue ear.
Chronic suppurative otitis media: foul discharge, ↓hearing, drum perforation
Infection spread: mastoiditis, petrositis, labyrinthitis, meningitis.
Facial palsy.
Abscess
Diabetic ketoacidosis (DKA)
Def, path, cause, class, sx, ix, mx, comp
An acute, severe manifestation of insulin deficiency, usually due to type 1 diabetes.
Pathophysiology
↓↓Insulin leads to:
↑Glucose
↑Ketones
↓pH and ↓HCO3-
Dehydration from polyuria and vomiting → renal impairment.
Causes:
Poor diabetic control.
Illness: infection, surgery, MI.
Insulin pump failure.
Severity classification
Classification by pH:
<7.3: mild.
<7.2: moderate.
<7.1: severe.
Signs and symptoms
Symptoms:
Nausea and vomiting. Due to gastroparesis and attempt to remove H+.
Abdo pain.
Polydipsia+uria
Lethargy
↓Level of consciousness.
Signs:
↓BP
↑HR
Dehydration
Kussmaul’s (deep) breathing to compensate for acidosis.
Ketone smell on breath.
Signs of cause e.g. infection.
Diagnosis and investigations
Criteria (all 3 required):
Capillary glucose >11 mmol/L or known diabetes.
Capillary/serum ketones ≥3 or urine 2+.
Venous pH <7.3 or HCO3- <15.
Other investigations:
↑Urea + Creatinine
Altered electrolytes: mostly ↓ as lost in urine. Exception is ↑K+ in ⅓, as though there is a low body total, it is ↑ in ECF due to ↓insulin, ↑osmolality, and acidaemia. Will drop after patient is given insulin.
↑Anion gap
↑Osmolality
↑WCC, even if no infection.
↑Amylase
Management
1. Normal saline through large bore cannula:
If SBP <90, give 500ml/15mins, and repeat if required.
If/when SBP >90, give 1L/1hr, then 1L/2hr x 2 (i.e. 2L/4hr), then 1L in 4h x 2, then 1L in 6h.
Summary: ‘½ in ¼ if <90, then 1L in 122446’.
2. K+ IV if <5.5 mmol/L:
Don’t include in first bag of fluids. Dehydration may cause AKI so that should be treated first.
If K+ <3.5, stop insulin until K+ normalised.
3. Insulin IV: 0.1 unit/kg/hr. 50 units short/rapid acting insulin in bag with normal saline made up to 50 ml. If glucose remains high (>7) after 2 hours, increase dose.
4. Assess patient and carry out investigations, including a septic screen (at least FBC and CXR). Consider HDU transfer if severe:
Ketones >6
K+ <3.5
GCS <12
Acid-base: HCO3-<5, pH <7.1, anion gap >16.
Vitals: O2 <92%, SBP <90, HR <60 or >100
5. Monitor:
Continuous O2 sats and ECG.
Every hour: capillary glucose should drop 3/hr, ketones should drop 0.5/hr, venous blood gas (HCO3- should rise 3/hr).
U&E should be done initially, then 2-hourly, then 4-hourly.
6. 10% glucose, 125 ml/hr, when glucose <14 and then continue until patient is eating.
7. Resolution should be seen within 24h, when ketones <0.3 and venous pH >7.3:
Once eating and drinking, switch to subcutaneous insulin, overlapping for first 30 mins with IV. Give short acting insulin with meals.
Complications
DKA itself:
VTE and PE.
Iatrogenic:
Cerebral oedema, mainly in children. If signs/symptoms develop – headache, altered mental status, pupillary/oculomotor abnormalities, unexpected ↑BP/↓HR, apnoea – treat with mannitol or hypertonic saline.
Hypokalaemia
Hypoglycaemia
Sepsis
Path, sx, mx, ix
Life-threatening organ dysfunction caused by a dysregulated host response to infection.
Pathophysiology
Pathogen recognition by immune cells – e.g. LPS-LBP endotoxin recognised by macrophages – leads to release of inflammatory mediators including TNFα, IL-1, and IL-6. This becomes generalised and eventually results in widespread cytokine activation.
Cytokines and inflammatory mediators lead to vasodilation, causing a distributive shock.
Microcirculatory failure and tissue hypoperfusion results from (a) inflammatory endothelial dysfunction and (b) an imbalance of coagulative and fibrinolytic mechanisms causing microvascular thrombosis, which may generalise to DIC.
Positive blood cultures support the diagnosis but are not required, and are only found in 1/3. Staph. aureus, Strep. pneumo, and Gram negative bacilli are the commonest pathogens.
Signs and symptoms
General signs include fever or ↓temperature, plus signs of distributive shock and organ hypoperfusion:
Abnormal obs: ↓BP, ↑HR, ↑RR.
Skin and peripheral changes: ↑cap refill, warm and sweaty and/or cold peripheries, mottled skin, petechial rash.
↓Urine output.
Altered mental status (also reflects delirium).
Local infection signs:
Pneumonia
Cellulitis
UTI
Meningitis
Peritonitis
However, there may be no obvious focal source.
Management
Initial investigations and treatment should ideally be completed within 1 hour, based on clinical suspicion and not requiring rigorous adherence to formal definitions.
Investigations:
Cultures of blood and other fluids e.g. urine, CSF.
Bloods: lactate (key marker of severity), Hb, U&E (AKI), LFT (liver dysfunction, potential biliary source), coag (DIC), and glucose.
Measure and record fluid balance inc. urine output (consider urinary catheter).
Once initial tests done, imaging to look for source, guided by history and exam e.g. CXR, US abdomen, CT abdo-pelvis.
Initial treatment:
IV antibiotics post-blood cultures. Broad spectrum – e.g. piperacillin/tazobactam – until blood culture results.
Fluids: start with 250-500 ml crystalloid challenge, and continue up to 30 ml/kg (≈ 2L for most), though some may need less or more.
Further treatment:
Vasopressors for fluid-refractory shock: noradrenaline is typically 1st line, with vasopressin and adrenaline as further options.
Steroids (e.g. hydrocortisone) may be used in vasopressor-refractory shock, though evidence is mixed.
Source control e.g. surgery to remove gallbladder or drain abscess.
Subdural haemorrhage
Sx, rx
Commonest type of bleed in traumatic head injury.
Signs and symptoms
Drowsy
Physical or cognitive slowing, personality changes.
Nausea and vomiting
↑Signs of ICP.
Urine incontinence (also suggests normal pressure hydrocephalus).
Can be acute or chronic, the latter not presenting until weeks or months post trauma.
Risk factors
3As:
Age
Anticoagulation
Alcohol
Breath holding and reflex anoxic seizure
Cause, sx
- Paroxysmal
- Caused by temporary decrease in cerebral blood flow due to reflex asystole or bradycardia
Anaphylaxis
Sx, mx
Immediate administration of adrenaline (1:1000, IM):
• Child > 12 years: 500 micrograms IM (0.5 mL)
• Child 6-12 years: 300 micrograms IM (0.3 mL)
• Child 6 months - 6 years: 150 micrograms IM (0.15 mL)
• Child < 6 months: 100-150 micrograms IM (0.1-0.15 mL)
Tonsillitis
Cause, sx, mx
The most common cause of tonsillitis is a viral infection. The most common cause of bacterial tonsillitis is group A streptococcus (Streptococcus pyogenes). This can be effectively treated with penicillin V (phenoxymethylpenicillin). The most common cause of otitis media, rhinosinusitis and the most common alternative bacterial cause of tonsillitis is Streptococcus pneumoniae.
Sx:
- fever
- sore throat
- painful swallowing
- headache
- vomiting
- red, inflamed and enlarged tonsils
- exudates
Centor (bacterial):
Fever over 38ºC
Tonsillar exudates
Absence of cough
Tender anterior cervical lymph nodes (lymphadenopathy)
Mx:
Antibiotics if centor score >3
clarithromycin as penicillin allergy alternative
The indications for tonsillectomy in recurrent tonsillitis are seven or more episodes in a single year, five or more episodes/year in two years, or three or more episodes/year in three years
Dehydration
classification
ADHD
Sx, mx
Sx:
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
Mx:
Healthy diet and exercise
Methylphenidate (“Ritalin“)- first line
Dexamfetamine
Atomoxetine
Autism spectrum disorder (ASD)
Sx, dx, mx
Sx:
- 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 (i.e. not playing with others)
- Communication
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
- Behaviour
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
Dx:
Paediatrician or paediatric psychiatrist
Mx:
Child psychology and child and adolescent psychiatry (CAMHS)
Speech and language specialists
Dietician
Paediatrician
Social workers
Specially trained educators and special school environments
Charities such as the national autistic society
Precocious puberty
Def, causes, sx, dx, mx
Precocious puberty refers to the early onset of puberty, typically defined as:
• Girls: Before age 8. • Boys: Before age 9.
Causes:
1. Central precocious puberty (gonadotropin-dependent): The most common form, caused by early activation of the hypothalamus-pituitary-gonadal axis, leading to the premature release of sex hormones.
• Often idiopathic (unknown cause), but may be linked to:
• Brain tumors or abnormalities.
• Genetic conditions or family history.
• Central nervous system infections or trauma.
2. Peripheral precocious puberty (gonadotropin-independent): Caused by the overproduction of sex hormones (estrogen or testosterone) from sources other than the brain, such as:
• Ovarian or testicular tumors.
• Adrenal gland disorders (e.g., congenital adrenal hyperplasia).
• Exposure to external sources of sex hormones (medications, creams).
Sx:
• Girls: Breast development, pubic hair, menstruation.
• Boys: Enlarged testicles and penis, facial hair, deepening of voice.
• Rapid growth and early growth spurts, followed by a shorter adult height due to early closure of growth plates.
Dx:
• Physical exam: Identifying the presence of secondary sexual characteristics.
• Blood tests: To measure hormone levels (FSH, LH, estradiol, testosterone).
• Imaging: MRI of the brain (to check for tumors or abnormalities), ultrasound (for ovarian or testicular tumors).
• Bone age X-rays: To check if bones are maturing too quickly.
Mx:
• GnRH analogs (gonadotropin-releasing hormone agonists): Medications used to pause early puberty by inhibiting the release of sex hormones, allowing the child to grow at a more typical pace.
• Surgery or other treatments: If a tumor or other abnormality is causing the early puberty.
Delayed puberty
Def, causes, sx, dx, mx
Delayed puberty refers to the absence of the onset of puberty by:
• Girls: Age 13 (no breast development or other signs of puberty).
• Boys: Age 14 (no testicular enlargement or other signs of puberty).
Causes:
1. Constitutional delay: The most common cause, where the child is a “late bloomer.” This condition often runs in families, and puberty eventually occurs without the need for treatment.
2. Hypogonadism (gonadotropin deficiency):
• Primary hypogonadism: The ovaries or testes fail to produce sufficient sex hormones due to conditions like Turner syndrome (in girls), Klinefelter syndrome (in boys), or damage to the gonads from chemotherapy, radiation, or infection.
• Secondary hypogonadism (central): Problems with the hypothalamus or pituitary gland, such as pituitary tumors, brain injuries, or chronic illnesses, can result in low production of the hormones that trigger puberty (FSH, LH).
3. Chronic medical conditions: Such as cystic fibrosis, diabetes, or malnutrition (e.g., from eating disorders), can delay puberty.
Sx:
• Lack of breast development or menstruation in girls.
• Lack of testicular enlargement or voice deepening in boys.
• Slower growth and development compared to peers.
Dx:
• Physical exam: Checking for signs of puberty.
• Family history: Delayed puberty often runs in families, particularly in cases of constitutional delay.
• Blood tests: To measure hormone levels (FSH, LH, estradiol, testosterone, thyroid hormones).
• Imaging: Bone age X-ray to assess bone development, and possibly an MRI of the brain or ultrasound of the reproductive organs to check for abnormalities.
Mx:
• Observation: If constitutional delay is the cause, no treatment may be necessary, and puberty will occur naturally.
• Hormone therapy: Short-term hormone replacement, such as low doses of testosterone for boys or estrogen for girls, may be given to jumpstart puberty if it is significantly delayed.
• Treating underlying conditions: Addressing any medical or hormonal issues that may be causing the delay, such as hypothyroidism or pituitary problems.
