Week 5

Question 1

Bacterial meningitis in infants

Answer 1

Bacteria that enter the bloodstream and travel to the brain and spinal cord cause acute bacterial meningitis. But it can also occur when bacteria directly invade the meninges. This may be caused by an ear or sinus infection, a skull fracture, or — rarely — some surgeries.

Several strains of bacteria can cause acute bacterial meningitis, most commonly:

Streptococcus pneumoniae (pneumococcus). This bacterium is the most common cause of bacterial meningitis in infants, young children and adults. It more commonly causes pneumonia or ear or sinus infections. A vaccine can help prevent this infection.

Neisseria meningitidis (meningococcus). This bacterium is another leading cause of bacterial meningitis. These bacteria commonly cause an upper respiratory infection but can cause meningococcal meningitis when they enter the bloodstream. This is a highly contagious infection that affects mainly teenagers and young adults. It may cause local epidemics. Even if vaccinated, anybody who has been in close contact with a person with meningococcal meningitis should receive an oral antibiotic to prevent the disease.

Haemophilus influenzae (haemophilus). Haemophilus influenzae type b (Hib) bacterium was once the leading cause of bacterial meningitis in children. But new Hib vaccines have greatly reduced the number of cases of this type of meningitis.

Listeria monocytogenes (listeria). These bacteria can be found in unpasteurized cheeses, hot dogs and lunchmeats. Pregnant women, newborns, older adults and people with weakened immune systems are most susceptible. Listeria can cross the placental barrier, and infections in late pregnancy may be fatal to the baby.

Question 2

Parasitic meningitis

Answer 2

Parasites can cause a rare type of meningitis called eosinophilic meningitis. Parasitic meningitis can also be caused by a tapeworm infection in the brain (cysticercosis) or cerebral malaria. Amoebic meningitis is a rare type that is sometimes contracted through swimming in fresh water and can quickly become life-threatening. The main parasites that cause meningitis typically infect animals. People are usually infected by eating foods contaminated with these parasites. Parasitic meningitis isn’t spread between people.

Question 3

Purpura

Answer 3

Purpura is the result of hemorrhage into the skin or mucosal membrane. It may represent a relatively benign condition or herald the presence of a serious underlying disorder. Purpura may be secondary to thrombocytopenia, platelet dysfunction, coagulation factor deficiency or vascular defect.

Question 4

Pathogenesis of bacterial meningitis

Answer 4

The organisms that cause bacterial meningitis colonize the nasopharynx and, from there, they get into the blood stream. They enter the subarachnoid space by passing through endothelial cells (transcytosis), getting across the porous choroid plexus capillaries, or being carried by granulocytes. The CSF is an ideal medium for the spread of bacteria because it provides enough nutrients for their multiplication and has few phagocytic cells, and low levels of antibodies and complement. Initially, bacteria multiply uninhibited and can be identified in smears, cultures, or by ELISA detection of their antigens before there is any inflammation.

Bacterial toxins cause neuronal apoptosis, and cell wall lipopolysaccharide (endotoxin), released from bacteria, activates clotting causing disseminated intravascular coagulation (DIC). More severe injury results from the inflammatory response to bacteria. Cells of the innate immune system of the brain, located in the BBB, choroid plexus, and ependyma, detect bacteria and secrete cytokines, chemokines, and complement, which attract circulating granulocytes into the CSF.

Granulocytes and macrophages have powerful lysosomal enzymes and free radicals, which they use to kill bacteria, but have a short life span. As they lyse, these compounds are spilled and can destroy everything in their way. If neutrophils accumulate, they can damage brain tissue, nerves, and blood vessels.

Vasculitis and clotting cause cerebral infarcts. So, brain damage in bacterial meningitis is caused in part by the direct action of bacteria and in part by the antibacterial inflammatory response. The most dangerous complication of bacterial meningitis is increased intracranial pressure from cerebral edema. Cerebral edema may be vasogenic, from increased vascular permeability, cytotoxic from cerebral hypoxia, interstitial, from increased CSF volume, or a combination of all. Increased intracranial pressure, in turn, causes decreased cerebral perfusion, hypoxia/ischemia, and neuronal necrosis.

Question 5

Brain abscess

Answer 5

Brain abscess is a newly formed cavity in brain tissue, filled with pus. The bacteria that cause brain abscess spread from adjacent air sinuses or the middle ear, or via the blood stream from the lungs (bronchiectasis, lung abscess), or from the heart (bacterial endocarditis). Brain abscess may also develop after neurosurgical procedures and open head injuries. The location of the abscess corresponds to its source. Frontal sinusitis causes frontal lobe abscess, and mastoiditis temporal lobe abscess. Hematogenous abscesses are often multiple.

Question 6

High risk symptoms for child/baby with fever:

Answer 6

cyanosis, no response to social cues, appearing ill to professionals, does not wake to consciousness, weak or high pitched continuous cry, grunting, resp rate over 60, chest indrawing, reduced skin turgor, bulging fontanelle.

Question 7

intermediate risk symptoms for child/baby with fever:

Answer 7

pallor, little social response, no smile, wakes with difficulty, decreased activity, nasal flaring, dry mucous membranes, poor feeding, reduced urine output, rigors.

Question 8

Heart rates for 0-12 months, 12-24 months and 2-5 years

Answer 8

0-12m over 160bpm, 12-24m over 150bpm, 2-5 years over 140bpm.

Question 9

Features of kawasaki disease

Answer 9

Be aware of the possibility of Kawasaki disease in children with fever that has lasted 5 days or longer. Additional features of Kawasaki disease may include:

bilateral conjunctival injection without exudate

erythema and cracking of lips; strawberry tongue; or erythema of oral and pharyngeal mucosa

oedema and erythema in the hands and feet

polymorphous rash

cervical lymphadenopathy

Question 10

Sepsis 6

Answer 10

The Sepsis Six is the name given to a bundle of medical therapies and monitoring designed to reduce mortality in patients with sepsis. Six tasks including oxygen, cultures, antibiotics, fluids, lactate measurement and urine output.

Question 11

Pneumonia

Answer 11

Characterised by acute inflammation with intense infiltration of neutrophils in and around the alveoli and terminal bronchioles. The area might be consolidated by the inflammation and oedema that results.

Most commonly S. pneumoniae, S. aureus, mycoplasma pneumoniae, Haemophilus influenza.

Symptoms: cough, purulent sputum which may be blood-stained or rust-coloured, breathlessness, fever, malaise.
Diagnosis is unlikely if there are no focal chest signs and heart rate, respiratory rate and temperature are normal.
The elderly may present with mainly systemic complaints of malaise, fatigue, anorexia and myalgia. Young children may present with nonspecific symptoms or abdominal pain.
Signs: tachypnoea, bronchial breathing, crepitations, pleural rub, dullness with percussion.

Question 12

Criteria for hospital admission with pneumonia

Answer 12

A 4-point score system is used, one point for each of:
Confusion (abbreviated mental test score 8 or less, or new disorientation in person, place or time).
Respiratory rate 30 breaths/minute or more.
Systolic blood pressure below 90 mm Hg (or diastolic below 60 mm Hg).
Age 65 years or older.

Question 13

Pneumonia antibiotic treatments

Answer 13

Low-severity CAP:
Offer a five-day course of amoxicillin, reserving clarithromycin, erythromycin (in pregnancy) or doxycycline for patients allergic to penicillin or if atypical pathogen suspected. Stop antibiotic after five days.

For high-severity CAP a five-day course of co-amoxiclav with clarithromycin or erythromycin (in pregnancy) should be offered. The oral or intravenous route can be used. Obviously the latter may prove challenging in the community.
Levofloxacin orally or IV is an option for patients allergic to penicillin.

Macrolides, such as doxycycline, clarithromycin and erythromycin (the preferred option in pregnancy), have been shown to be effective in the treatment of all three most common infective organisms. They should be considered in all cases of pneumonia (including community-acquired) where atypical pathogens are suspected

Question 14

Complications of pneumonia

Answer 14

Pleural effusion that is usually sterile.
Empyema: a reactive effusion can occur but is trivial. Empyema is potentially more serious and presents as the persistence of fever and leukocytosis after 4-5 days of appropriate antibiotic therapy.
Lung abscess: can occur in disease due to S. pneumoniae and is classically seen in patients with klebsiella or staphylococcal pneumonia.
Pneumatocele.
Pneumothorax.
Pyopneumothorax - eg, following rupture of a staphylococcal lung abscess in the pleural cavity.
Deep vein thrombosis.
Septicaemia, pericarditis, endocarditis, osteomyelitis, septic arthritis, cerebral abscess, meningitis (particularly in pneumococcal pneumonia).
Postinfective bronchiectasis.
Acute kidney injury.

Question 15

Whooping cough

Answer 15

Whooping cough is a highly infectious notifiable disease caused by the bacterium Bordetella Pertussis.

Vaccines against pertussis are given at 2, 3 and 4 months of age, with a booster at 3 years and 4 months.

A gram-negative bacillus which spreads through aerosolised droplets produced by the cough of an infected individual. The bacteria attach to the respiratory epithelium and produce toxins which paralyse the cilia and promote inflammation, impairing the clearance of respiratory secretions, which leads to a cough. Is highly contagious.

Catarrhal phase lasts 1 to 2 weeks and produces symptoms including:

Rhinitis
Conjunctivitis
Irritability
Sore throat
Low-grade fever
Dry cough

Paroxysmal phase lasts for 2-8 weeks and has frequent bouts of coughing followed by whoop sound. By 3 months, this decreases and apnoea and vomiting until the convalescent phase.

If under a month old, give clarithromycin. That or azithromycin if over a month. Second line is cotrimoxazole.

Complications include:
 Secondary bacterial pneumonia (up to 20% of infants)
Seizures
Encephalopathy (rare)
Otitis media

Question 16

Causes of neonatal jaundice

Answer 16

Prematurity, maternal diabetes, polycythemia, infection/sepsis, hypothyroidism, biliary atresia, cystic fibrosis, Crigler-Najjar syndrome, Gilbert syndrome, hepatitis, thalassemia, and galactosemia.

Question 17

Bronchiolitis risk factors and clinical features

Answer 17

Being breast fed for less than 2 months
Smoke exposure (eg. parents’ smoke)
Having siblings who attend nursery or school (increased risk of exposure to viruses)
Chronic lung disease due to prematurity.

Question 18

Early onset neonatal sepsis

Answer 18

early-onset neonatal sepsis (occurring within the first 48-72 hours of life). Early-onset sepsis is caused by infection with organisms from the maternal genital tract.

Risk factors include prematurity, low birth weight, over 18hrs rupture of membranes in labour, maternal GBS, maternal infection during labour eg chorioamnionitis.

Most common causative agents are GBS, Ecoli and Listeria monocytogenes.

Treatment includes benzyl penicillin and gentamicin. Add cefotaxime if signs of gram negative infection.

Give amoxicillin and cefotaxime (IV) if meningitis is suspected
Add metronidazole if NEC is suspected
Add an antifungal (e.g. amphotericin B) if fungal sepsis is suspected (high-risk baby with a negative blood culture)
Add aciclovir (IV) if HSV infection is suspected (e.g. vesicular rash, late-onset sepsis with respiratory disease or sepsis not responding to antibiotics)

Question 19

Late onset neonatal sepsis

Answer 19

(occurring after the first 48-72 hours of life). late-onset sepsis is caused by organisms acquired through interaction with the home or hospital environment. Risk factors include prematurity, low birth weight, invasive procedures.

Coagulase-negative staphylococci (e.g. Staph. epidermidis) (~60%)

Staph. aureus (~6%)

E. coli (~6%)

Give Flucloxacillin (or vancomycin) plus gentamicin (IV).

Give amoxicillin and cefotaxime (IV) if meningitis is suspected
Add metronidazole if NEC is suspected
Add an antifungal (e.g. amphotericin B) if fungal sepsis is suspected (high-risk baby with a negative blood culture)
Add aciclovir (IV) if HSV infection is suspected (e.g. vesicular rash, late-onset sepsis with respiratory disease or sepsis not responding to antibiotics)

Question 20

Signs and complications of neonatal sepsis

Answer 20

Fever or temperature instability
Lethargy
Jaundice
Hypo- or hyperglycaemia
Apnoea
Respiratory distress
Cyanosis
Tachycardia or bradycardia
Hypotension
Poor perfusion and prolonged capillary refill
Poor feeding
Abdominal distention

Neurological (consider meningitis):
Irritability
Seizures
Bulging fontanelle

Complications of neonatal sepsis:

Poor cognitive development
Visual or hearing deficits
Cerebral palsy
Bronchopulmonary dysplasia (BPD)
Death

Question 21

Roseola

Answer 21

Roseola, also known as sixth disease, is an infectious disease caused by certain types of human herpes 6. Most infections occur before the age of three. Symptoms vary from absent to the classic presentation of a fever of rapid onset followed by a rash. The fever generally lasts for three to five days, while the rash is generally pink and lasts for less than three days, starting on torso. Complications may include febrile seizures, with serious complications being rare.

Question 22

Gianotti-Crosti Syndrome

Answer 22

Rash as a reaction to systemic viral infection between the age of 6-12m.

Hepatitis B infection
Epstein-Barr virus (EBV)
Cytomegalovirus (CMV)
Enterovirus infections
Echoviruses
Respiratory syncytial virus
SARS-CoV-2 (COVID-19).
Although originally described in children with hepatitis B, vaccination against this virus in most populations means EBV is now the most common association.

Papular acrodermatitis of childhood presents over the course of 3 or 4 days. A profuse eruption of dull red spots develops first on the thighs and buttocks, then on the outer aspects of the arms, and finally on the face. The rash is usually symmetrical.

The individual spots are 5–10 mm in diameter and are a deep red colour. Later they often look purple, especially on the legs, due to leakage of blood from the capillaries. They may develop fluid-filled blisters (vesicles).

Papular acrodermatitis of childhood is not usually itchy.

The child with papular acrodermatitis may feel quite well or have a mild temperature. Mildly enlarged lymph nodes in the armpits and groins may persist for months. When papular acrodermatitis is caused by hepatitis B, there may be an enlarged liver, but there is seldom any jaundice.

Question 23

Head shape abnormalities in babies

Answer 23

Cranial moulding is common after birth and resolves within a few days.

Caput succedaneum is a diffuse subcutaneous fluid collection with poorly defined margins (often crossing suture lines) caused by pressure on the presenting part of the head during delivery. It does not usually cause complications and resolves over the first few days.

Cephalhaematoma is a subperiosteal haemorrhage which occurs in 1-2% of infants and may increase in size after birth. The haemorrhage is bound by the periosteum, therefore, the swelling does not cross suture lines (in contrast to a caput succedaneum). Cephalhaematoma is more common with instrumental delivery and may cause jaundice, therefore, bilirubin should be monitored.

Subgaleal haemorrhages occur between the aponeurosis of the scalp and periosteum and form a large, fluctuant collection which crosses sutures lines. They are rare but may cause life-threatening blood loss.

Craniosynostosis is a condition in which one or more of the fibrous sutures in an infant skull prematurely fuses, changing the growth pattern of the skull which can result in raised intracranial pressure and damage to intracranial structures. Surgical intervention is required with the primary goal being to allow normal cranial vault development to occur. This can be achieved by excision of the prematurely fused suture and correction of the associated skull deformities.

Question 24

Examples of facial birthmarks and blemishes in newborns

Answer 24

Salmon patch (also known as a stork mark or nevus simplex): red or pink patches, often on an infant’s eyelids, head or neck caused by congenital capillary malformation. Salmon patches are very common and usually fade by the age of two.

Haemangiomas (also known as strawberry marks): blood vessels which form a raised red lump on the skin which appears soon after birth. Haemangiomas typically get bigger over the first 6-12 months and then shrink and disappear by the age of 7. They may require treatment if they affect vision, breathing or feeding.

Port-wine stain (also known as naevus flammeus): red/purple marks on the face and neck which are typically present from birth and do not regress. Port-wine stains can sometimes be associated with Sturge-Weber syndrome and Klippel-Trenaunay syndrome.

Slate-grey nevus is a benign, flat, congenital birthmark with wavy borders and irregular shape, usually located over the sacrum. It is most commonly blue in colour and can be mistaken for a bruise. They normally disappear within 3-5 years after birth.

Milia are tiny white cysts containing keratin and sebaceous material. They are very common on the face and most resolve within the first few weeks of life.

Erythema toxicum is a very common and benign condition seen in newborn infants. It presents with various combinations of erythematous macules, papules, and pustules. Lesions usually appear from 48 hours of age and resolve spontaneously.

Question 25

Cystic hygroma

Answer 25

A cystic hygroma is a congenital lymphatic lesion which is typically identified prenatally or at birth. A cystic hygroma can arise anywhere but typically develops in the left posterior triangle of the neck. Cystic hygromas are benign but can be disfiguring and typically require surgical treatment including drainage and use of sclerosing agents to prevent reaccumulation of lymphatic fluid.

Question 26

Cholesteatoma

Answer 26

A cholesteatoma is an abnormal sac of keratinizing squamous epithelium and accumulation of keratin within the middle ear or mastoid air cell spaces which can become infected and also erode neighbouring structures.

Cholesteatoma most commonly presents with a persistent or recurrent discharge from the ear that is often foul smelling. An associated conductive hearing loss may also occur.
Rarely with progression of the disease, vertigo, sensorineural hearing loss, facial nerve palsy, meningitis, or intracranial abscess may develop.

The diagnosis requires clear visualisation of the tympanic membrane. If the tympanic membrane can be seen, a cholesteatoma should be suspected if there is:
Evidence of ear discharge.
Presence of a deep retraction pocket, with or without granulation tissue and skin debris.
Crust or keratin in the upper part of the tympanic membrane.
The tympanic membrane may be perforated.
Congenital cholesteatoma (rare) may appear as a white mass behind an intact tympanic membrane, in a person with no prior history of ear discharge, tympanic membrane perforation, or surgical procedures on the ear.

If there is significant discharge occluding the tympanic membrane, referral for examination with an otomicroscope and micro-suctioning of the ear may be appropriate. Alternatively, clinical judgement should be used to decide whether to treat for presumed infection, in which case the person should be treated for either:
Otitis externa, particularly if there are symptoms and signs of inflammation of the external auditory canal, or
Acute otitis media if there has been an acute onset of pain associated with the purulent discharge.

Question 27

Arachnoid Cysts

Answer 27

Arachnoid cysts are fluid-filled sacs that occur on the arachnoid membrane that covers the brain (intracranial) and the spinal cord (spinal). There are three membranes covering these parts of the central nervous system: the dura mater, arachnoid, and pia mater. Arachnoid cysts appear on the arachnoid membrane, and they may also expand into the space between the pia mater and arachnoid membranes (subarachnoid space). The most common locations for intracranial arachnoid cysts are the middle fossa (near the temporal lobe), the suprasellar region (near the third ventricle) and the posterior fossa, which contains the cerebellum, pons, and medulla oblongata.

In many cases, arachnoid cysts do not cause symptoms (asymptomatic). In cases in which symptoms occur, headaches, seizures and abnormal accumulation of excessive cerebrospinal fluid in the brain (hydrocephalus) are common.

The most common symptoms associated with arachnoid cysts are usually nonspecific and include headaches, nausea, vomiting, dizziness and the accumulation of excessive cerebrospinal fluid in the brain (hydrocephalus), resulting in increased intracranial pressure In rare cases, in some children, an arachnoid cyst can cause malformation of certain cranial bones, resulting in an abnormally enlarged head (macrocephaly). .

A variety of additional symptoms occur in some individuals with arachnoid cysts depending upon the size and location of the cyst. Most cysts occur near the middle fossa region of the brain. Such symptoms include lethargy, seizures, vision abnormalities and hearing abnormalities. Neurological signs may be present because arachnoid cysts may cause increased pressure on structures of the brain. Such neurological findings may include developmental delays, behavioral changes, an inability to control voluntary movements (ataxia), difficulties with balance and walking and cognitive impairment. Weakness or paralysis on one side of the body (hemiparesis) has also been reported.

In addition to hydrocephalus, cysts located in the suprasellar region may be associated with vision disturbances, continuous bobbing of the head, and abnormalities affecting certain hormone-producing glands that help to regulate the rate of growth, sexual development, and certain metabolic functions (endocrine system).

Although they occur much less often than those found within the skull (intracranial), arachnoid cysts may also arise near the spine (spinal arachnoid cysts). Spinal arachnoid cysts may be associated with progressive weakness of the legs, tingling or numbness in the hands or feet, abnormal side-to-side curvature of the spine (scoliosis), back pain, and involuntary muscle spasms (spasticity) that result in slow, stiff movements of the legs. In rare cases, these cysts may cause paralysis of the legs (paraplegia). Urinary tract infections may also occur in individuals with spinal arachnoid cysts.

In cases where treatment is recommended, therapy traditionally consists of one of two procedures – an open craniotomy fenestration or ventriculoperitoneal shunting.

Question 28

Pierre Robin Sequence

Answer 28

The typical features of PRS are:

Micrognathia or retrognathia (small or retracted mandible).
Cleft palate (classically U-shaped but V-shaped may occur, usually without cleft lip).
Glossoptosis (implying a relatively large tongue. In reality, the tongue may be normal size or small, so upper airway obstruction may be substituted for this feature).

Neonates with severe micrognathia present as emergencies at birth with significant respiratory obstruction, requiring a nasopharyngeal airway or intubation.
Affected babies are at risk of obstructive sleep apnoea. Unrecognised or untreated airways obstruction may lead to chronic hypoxia and cerebral impairment, failure to thrive and cor pulmonale.
The most common early problem is feeding difficulties, as the cleft palate prevents enough negative pressure to feed effectively.
Careful examination for other somatic abnormalities, including examination of the eyes and ears, may indicate the presence of the malformation as one of the related syndromes. EG fetal alcohol syndrome, stickler’s syndrome: PRS plus severe myopia, retinal detachment and blindness with abnormal epiphyseal development due to alpha-1 collagen II polypeptide mutation.
Velocardiofacial syndrome: 22q deletion with neuropsychiatric impairments and cardiac abnormalities.

Treatments may include distraction jaw osteogenesis, tongue-lip adhesion/glossopexy and tracheostomy.

Question 29

Juvenile myoclonic epilepsy

Answer 29

Juvenile myoclonic epilepsy is an epilepsy syndrome characterized by myoclonic jerks (quick jerks of the arms or legs), generalized tonic-clonic seizures (GTCSs), and sometimes, absence seizures. The seizures often occur when people first awaken in the morning. Seizures can be triggered by lack of sleep, extreme fatigue, stress, or alcohol consumption. Onset typically occurs around adolescence in otherwise healthy children. Might self resolve in middle adulthood.

The signs and symptoms of juvenile myoclonic epilepsy are:
Myoclonic jerks or seizures, which are described as quick jerks of the arms and legs, and are the hallmark feature of the disease; they may be the only symptom in about 17% of the cases; in about 20% of the cases, the seizures occur in clusters, affecting only one side (unilateral) of the body, and start before a tonic-clonic seizure
Generalized tonic-clonic seizures, appear a few months after onset of myoclonic jerks
Absence seizures, usually the first symptom to present around 5 and 16 years of age
Myoclonic status epilepticus is considered to be the most concerning problem of juvenile myoclonic epilepsy. It occurs when multiple myoclonic seizures do not readily stop and after sleep deprivation or missing medications.

Anti-convulsants are typically needed and well tolerated. The majority of patients can be well-controlled on a single drug, most commonly valproic acid. Other medications that might be used separately or in combination include lamotrigine, levetiracetam, clonazepam, and topiramate.

Question 30

Encephalopathy

Answer 30

It is a term to describe brain dysfunction. Thus there are many types. The primary symptom in all is an altered mental state. It can be cause by infection, alcohol toxicity, trauma, liver and kidney failure, hypoxia/reduced cerebral perfusion, metabolic disorders and malnutrition.

Other symptoms can involve memory loss, lack of concentration, cognitive decline, loss of consciousness, muscle twitches, REM, muscle weakness, seizures.

Question 31

Common malignant and benign brain tumour types

Answer 31

Metastatic

The most common brain tumor among adults, metastatic tumors are classified as secondary brain tumors, which means they arise from cancer that formed elsewhere in the body and then spread to the brain. Metastatic tumors most often stem from lung or breast cancer. Larger metastatic tumors will often be surgically resected and smaller tumors may be treated with a gamma knife.

2. Meningioma

These tumors are technically not brain tumors, as they form in the meninges, which are the membranes that line the skull and vertebral canal. But their growth may affect the brain by causing various disabilities such as vision and hearing impairment, memory loss or seizures. Incidents of meningioma increase with age, and the tumors grow slowly, so symptoms could develop gradually over time. They are benign. The most common early sign of meningioma is chronic headaches but often they can be asymptomatic.

3. Glioblastoma

Glioblastoma is the most common primary brain tumor, which means it originates in the brain. It has the worst prognosis. Treatment includes surgical resection, radiation therapy, and chemotherapy. Currently, the aim is to employ immunotherapy trials. Immunotherapy basically reprograms a patient’s immune system to target and attack cancer cells.

4. Astrocytoma

These primary tumors originate in astrocytes, starting from the brain’s cerebrum. The grade of astrocytoma tumors varies; sometimes they grow slowly (Grade II) and sometimes they come on more aggressively (Grade III). Treatment approaches to astrocytomas always involve surgery, and occasionally involve chemotherapy and radiation therapy. Astrocytomas have more positive overall survival rates.

On the whole, persistent headaches are the most common early signs of brain tumors. Some warning signs would be headaches that increase in frequency and intensity over days and weeks, and if the headaches become so intense that it wakes up a sleeping patient.

Question 32

Larynx

Answer 32

The arterial supply to the larynx is via the superior and inferior laryngeal arteries:

Superior laryngeal artery – a branch of the superior thyroid artery (derived from the external carotid). It follows the internal branch of the superior laryngeal nerve into the larynx.

Inferior laryngeal artery – a branch of the inferior thyroid artery (derived from the thyrocervical trunk). It follows the recurrent laryngeal nerve into the larynx.

Venous drainage is by the superior and inferior laryngeal veins. The superior laryngeal vein drains to the internal jugular vein via the superior thyroid, whereas the inferior laryngeal vein drains to the left brachiocephalic vein via the inferior thyroid vein.

Innervation

The larynx receives both motor and sensory innervation via branches of the vagus nerve:

Recurrent laryngeal nerve – provides sensory innervation to the infraglottis, and motor innervation to all the internal muscles of larynx (except the cricothyroid).

Superior laryngeal nerve – the internal branch provides sensory innervation to the supraglottis, and the external branch provides motor innervation to the cricothyroid muscle.

Anatomically, the internal cavity of the larynx can be divided into three sections:

Supraglottis – From the inferior surface of the epiglottis to the vestibular folds (false vocal cords).

Glottis – Contains vocal cords and 1cm below them. The opening between the vocal cords is known as rima glottidis, the size of which is altered by the muscles of phonation.

Subglottis – From inferior border of the glottis to the inferior border of the cricoid cartilage.

The interior surface of the larynx is lined by pseudostratified ciliated columnar epithelium. An important exception to this is the true vocal cords, which are lined by a stratified squamous epithelium.

The laryngeal membranes and ligaments support the cartilaginous skeleton of the larynx.

The extrinsic ligaments act to attach the components of the larynx to external structures (such as the hyoid and the cricoid cartilage). The intrinsic ligaments are responsible for holding the cartilages of the larynx together as one functional unit internally

Extrinsic:

Thyrohyoid membrane – Spans between the superior aspect of the thyroid cartilage and the hyoid bone. It is pierced laterally by the superior laryngeal vessels and internal laryngeal nerve (branch of the superior laryngeal nerve).

Median thyrohyoid ligament – Anteromedial thickening of the membrane.

Lateral thyrohyoid ligaments – Posterolateral thickenings of the membrane.

Hyo-epiglottic ligament – Connects the hyoid bone to the anterior aspect of the epiglottis.

Cricotracheal ligament – Connects the cricoid cartilage to the trachea.

Median cricothyroid ligament – Anteromedial thickening of the cricothyroid ligament (see below), connecting the thyroid and cricoid cartilages.

Intrinsic:

Cricothyroid ligament – Originates from the cricoid cartilage and extends superiorly, where it terminates with an free (unattached) upper margin – which forms the vocal ligament. It is additionally attached anteriorly to the thyroid cartilage, and posteriorly to the arytenoid cartilage.

Quadrangular membrane – Spans between the anterolateral arytenoid cartilage and the lateral aspect of the epiglottis. It has a free upper margin and lower margin. The lower margin is thickened to become the vestibular ligament.

The vocal folds (true vocal cords) are the more important of the two sets. Under the control of the muscles of phonation, they are abducted, adducted, relaxed and tensed to control the pitch of the sound created.

Vocal ligament – Lies at the free upper edge of the cricothryoid ligament.

Vocalis muscle – Exceptionally fine muscle fibres that lie lateral to the vocal ligaments.

The vocal folds are relatively avascular, and appear white in colour. The space between the vocal folds is known as the rima glottidis.

The vestibular folds (false vocal cords) lie superiorly to the true vocal cords. They consist of the vestibular ligament (free lower edge of the quadrangular membrane) covered by a mucous membrane, and are pink in colour. They are fixed folds, which act to provide protection to the larynx.

Question 33

Viral gastroenteritis

Answer 33

Symptoms (remote and face-to-face assessments)
sudden vomiting and diarrhoea. often bloody.

Likely dehydrated if:
Well child Perceived to be unwell or deteriorating
Normal conscious state Excessive or unaccustomed irritability
or lethargy
Depressed conscious
state
Normal level of thirst Increased thirst
Normal urine outputb Decreased urine outputb
Normal skin colour Normal skin colour Pale or mottled skin
Warm hands and feet Warm hands and feet Cold hands and feet
Signs (face-to-face assessments only)
Normal conscious state Irritability or lethargyDepressed conscious
state
Clinical feature of dehydration
Normal skin colour and
warm peripheries
Normal skin colour and warm
peripheries
Pale or mottled skin
and/or cold peripheries

In children with clinical dehydration, including hypernatraemic dehydration:
− treat with low osmolarity ORS
− give 50 ml/kg of ORS over 4 hours in addition to maintenance fluids
− administer the fluid frequently and in small amounts
− consider supplementation with their usual fluids (including milk feeds or
water, but not fruit juices) if they refuse to take adequate quantities of
ORS and do not have red flag symptoms or signs of dehydration
− consider administration of ORS via nasogastric tube if they are unable to
drink ORS or vomit persistently
− monitor the response to ORT by regular clinical reassessment.
• Use intravenous fluid therapy (IVT) for dehydration:
− if clinical assessment confirms or raises suspicion of shock
− if, despite appropriate ORT, there are signs of deterioration with red flag
symptoms or signs of dehydration
• Following rehydration:
− give full-strength milk from the outset
− reintroduce the child’s usual solid food
− avoid giving fruit juice until diarrhoea has stopped

Question 34

Meniere’s disease

Answer 34

Meniere’s disease is a disorder affecting the inner ear which can affect balance and hearing.
It is a clinical syndrome characterized by episodes of vertigo, fluctuating hearing loss, and tinnitus and is associated with a feeling of fullness in the affected ear.
The cause of Meniere’s disease is not known but it may be associated with endolymphatic hydrops (raised endolymph pressure in the membranous labyrinth of the inner ear).

Meniere’s disease is associated with complications of falls, adverse psychological impact and social effects.
Suspect Meniere’s disease if the person has classic symptoms of episodes of spontaneous vertigo, tinnitus, fluctuating sensorineural hearing loss, and aural fullness.
Initially, symptoms of Meniere’s disease fluctuate, resolving between episodes. Progression results in further hearing loss and persistent tinnitus. Eventually, vertigo symptoms may resolve, but the person may have residual hearing loss and tinnitus.

short course of prochlorperazine or an antihistamine (for example cinnarizine, cyclizine, or promethazine teoclate) should be considered.
If symptoms are severe enough, people may require hospital admission for intravenous (IV) labyrinthine sedatives and fluids to maintain hydration and nutrition.
A trial of betahistine can be considered to reduce the frequency and severity of attacks.

Question 35

Breath Sounds

Answer 35

Normal breath sounds are classified as bronchial, vesicular, or bronchovesicular, which have different acoustic properties based on anatomical characteristics of the location where you are auscultating. Bronchial sounds (also called tubular sounds) normally arise from the tracheobronchial tree and vesicular sounds normally arise from the finer lung parenchyma. Loud, harsh, and high pitched bronchial sounds are typically heard over the trachea or at the right apex. They are predominantly heard during expiration. If heard in other areas of the lung, bronchial sounds are abnormal. In contrast, vesicular breath sounds are soft, low pitched, predominantly inspiratory, and appreciated especially well at the posterior lung bases. Bronchovesicular sounds can be heard during inspiration and expiration and have a mid-range pitch and intensity. They are commonly heard over the upper third of the anterior chest.

Question 36

Adventitious Sounds

Answer 36

Crackles, rhonchi, and wheezes. Stridor and rubs.

Question 37

Lobar consolidation

Answer 37

For example, bronchial (loud & tubular) breath sounds are abnormal in peripheral areas where only vesicular (soft & rustling) sounds should be heard. When bronchial sounds are heard in areas distant from where they normally occur, the patient may have consolidation (as occurs with pneumonia) or compression of the lung. These conditions cause the lung tissue to be dense. The dense tissue transmits sound better from the lung bronchi.

Question 38

Crackles (or rales)

Answer 38

caused by fluid in the small airways or atelectasis. Crackles are referred to as discontinuous sounds; they are intermittent, nonmusical and brief. Crackles may be heard on inspiration or expiration. The popping sounds produced are created when air is forced through respiratory passages that are narrowed by fluid, mucus, or pus. Crackles are often associated with inflammation or infection of the small bronchi, bronchioles, and alveoli. Crackles that don’t clear after a cough may indicate pulmonary edema or fluid in the alveoli due to heart failure or adult respiratory distress syndrome (ARDS).

Fine (popping bubbles) are typically late inspiratory and coarse are usually early inspiratory

Medium crackles are high pitched, very brief and soft. It sounds like rolling a strand of hair between two fingers. Fine crackles could suggest an interstitial process; e.g pulmonary fibrosis, congestive heart failure.

Coarse crackles (velcro sound) are louder, more low pitched and longer lasting. They indicate excessive fluid on the lungs which could be caused by aspiration, pulmonary oedema from chronic heart disease, chronic bronchitis, pneumonia

Overall list of causes:
Pneumonia
Heart disease
Pulmonary fibrosis
Cystic fibrosis
COPD
Lung infections, like bronchitis or bronchiolitis
Asbestosis, a lung disease caused by breathing in asbestos
Pericarditis, an infection of the sac that covers your heart

Question 39

Wheeze

Answer 39

Wheezing is a term used to describe high whistling sounds in the lungs, and it is usually more pronounced with expiration. Or during both inspiration and expiration. They are caused by air moving through airways narrowed by constriction or swelling of airway or partial airway obstruction.

Two of the most common causes of wheezing are lung diseases called chronic obstructive pulmonary disease (COPD) and asthma. But many other issues can make you wheeze, too, including:

Allergies
Bronchitis or bronchiolitis
Emphysema
Epiglottitis (swelling of the top flap of your windpipe)
Gastroesophageal reflux disease (GERD)
Heart failure
Lung cancer
Sleep apnea
Pneumonia
Respiratory syncytial virus (RSV)
Vocal cord problems
An object stuck in your voice box or windpipe

Rhonchi- low pitched wheeze They often clear with coughing and are usually caused by an obstruction or build-up of mucus in the large airways.
Squawks- Short inspiratory wheeze conditions such as pneumonia, lung fibrosis, or bronchiolitis obliterans.

Question 40

Stridor

Answer 40

Stridor is a high-pitched sound originating from the upper airway and occurring on inspiration. It is distinguished from other sounds by its intensity in the neck more so than the chest, timing (inspiratory), and pitch (high). Like wheezes, stridor is produced by airway narrowing, but only in the upper airways. Risk for obstruction.

Laryngomalacia (softening of the vocal cords in babies)
Paralyzed vocal cord
Narrow voice box
Macroglossia/micrognathia
Unusual growth of blood vessels (hemangioma) just below your vocal cords
Croup (Laryngotracheobronchitis)
Laryngitis
Epiglottitis
Anaphylaxis
You can also have stridor if an object gets stuck in your windpipe.

Question 41

Pleural Rub

Answer 41

A rub is a raspy grating sound coming from inflamed pleura rubbing against one another. It is usually louder than other lung sounds due to its generation closer to the chest wall. Rubs usually occur during both inspiration and expiration at a mirrored point in the respiratory cycle. Rubs are most often confused with crackles but are distinguished by the rub’s biphasic, localized quality, often with overlying point pain on the chest wall.

Pleurisy
Lung tumors that extend to the pleura
Pleural mesothelioma (a malignant tumor of the pleura)
Pneumonia
Pulmonary embolism

Pleural friction rubs are low-pitched, grating, or creaking sounds that occur when inflamed pleural surfaces rub together during respiration. More often heard on inspiration than expiration, the pleural friction rub is easy to confuse with a pericardial friction rub. To determine whether the sound is a pleural friction rub or a pericardial friction rub, ask the patient to hold his breath briefly. If the rubbing sound continues, its a pericardial friction rub because the inflamed pericardial layers continue rubbing together with each heart beat - a pleural rub stops when breathing stops.

Question 42

Fine vs coarse crackles/rales

Answer 42

Coarse crackles: originates within large bronchial tubes. Heard in consolidation, lung cavitation, abscess, pulmonary congestion or oedema and bronchiectasis.

Fine crackles: localised sound made louder on coughing. Due to sticking of alveolar walls. Characteristic of early pneumonia, atelectasis, bronchitis, bronchiolitis, pulmonary oedema.

Tracheal Rales/Death Rattle- heard over trachea or lungs of seriously ill who can’t expectorate.