Pathology 8 Flashcards

1
Q

Scarlet fever

A

Scarlet fever is an exotoxin-mediated disease arising from a specific bacterial infection by an erythrogenic (causing inflammation and reddening of the skin) toxin-producing strain of Streptococcus pyogenes

Pathophysiology
•In most cases scarlet fever evolves from a tonsillar or pharyngeal infection
•Person-to-person spread is mainly by respiratory droplets. The incubation is typically 2 to 5 days but ranges from 1 to 7 days.
•Patients are contagious both during the acute illness and the initial subclinical stage

Epidemiology
• 87% children are aged under 10 years with a median age of 4 years. Scarlet fever is unusual under the age of 2 years because of maternal antibodies to the exotoxin and lack of prior sensitisation.
•The infection rate increases with overcrowding and close contact. School populations have a higher incidence
•Incidence decreases in adults as immunity develops.

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2
Q

Scarlet fever management

A

Treatment

•Antibiotics. Penicillin or azithromycin if penicillin-allergic are the treatments of choice given for a full 10 days.

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3
Q

Signs of meningitis

A
Signs and symptoms of may include:
◾Fever
◾Headache
◾Nausea
◾Vomiting
◾Sleepiness
◾Irritability
◾Stiff neck
◾Seizures
◾Photophobia
CLASSIC TRIAD
•Bulging fontanelle (in infants)
•Altered mental state, unconsciousness, toxic/moribund state.
•Unusual skin colour, capillary refill time more than 2 seconds; cold hands/feet.
•Tachycardia and/or hypotension; respiratory symptoms or breathing difficulty.
•Leg pain
•Poor urine output
•Haemorrhagic rash (a type of rash caused by bleeding underneath the skin)

Signs
•Kernig’s sign (pain and resistance on passive knee extension with hips fully flexed).
•Brudziñski’s sign (hips flex on bending the head forward).
Timing of symptoms
• Classical signs such as haemorrhagic rash, the triad and impaired consciousness did not tend to appear until after 13 to 22 hours.
•More nonspecific features such as leg pain, cold hands and feet and abnormal skin colour appeared much earlier with a median onset of 7-12 hours.
•These earlier features are therefore very important in early diagnosis and therefore in the earlier initiation of potentially life-saving treatment

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4
Q

APGAR score

A

This is the first test given to newborns after birth.

  • Used to assess the condition of the newborn.
  • Usually done at 1 and 5 minutes after birth. However, if there is still some concern then it maybe repeated after 10 minutes.
  • APGAR is an acronym that stands for: Appearance, Pulse >100, Grimace?, Activity and Respiration.

Appearance: Is the look of the baby, especially noting the colour of the baby’s skin. This is a good indicator of how good a baby’s circulation is.
Pulse: Is the Heart rate of the newborn.
Grimace: Is how the baby reacts to stimulation. This stimulation is usually a pinch on the arm or a rub on the sternum (chest wall) to stimulate mild pain.
Activity: This is how much the baby is moving and general muscle tone
Respiration: Is not only how fast a baby is breathing but also how much effort the baby is putting in and how regular the breathing is. A baby’s cry is a very good indicator of how well the baby is breathing.

score from 0-2 for each category out of ten together. 7-9 is normal.

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5
Q

Measles incubation period and development

A

-Incubation period is between 8-14 days. An incubation period is the time period between first coming into contact with the pathogen and the pathogen causing symptoms.

The clinical features of measles can be split into a pre eruptive and eruptive stage (Basically a stage before the rash and a stage once the rash has developed).
Pre-eruptive: Malaise, fever, runny nose, cough and conjunctivitis (Redness and irritation of the eyes). During this acute illness there are many viruses being shed and spread in the droplets so the person is most infective during this period.
A more diagnostic sign is the appearance of koplik’s spots. These are greyish spots that appear on the buccal membrane (on the cheek) a say or two after the flu-like symptoms and a day or two before the rash appears.
Eruptive: The rash usually appears 3-4 days after the general symptoms.
The rash begins on the face usually on the forehead (or below the hairline, depending which sources you believe) and then spreads down the rest of the body.
The rash is maculopapular in nature. The rash is characterized by flat, red areas on the skin covered by confluent bumps.
The rash usually fades after a week, but may leave some scaring towards the end in severe cases.

School exclusion: children with measles should be kept out of school and isolated as much as possible for at least 5 days after the rash begins.

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6
Q

Mumps complication

A

Complications: In pre-pubertal males the virus can cause Orchiditis (inflammation of the testes). The most severe complication occurs if the virus enters the meninges (protective layer over spinal cord/brain), causing meningitis; this occurs in about 5% of cases.

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7
Q

Rubella presentation

A

-Incubation period varies from 2-3 weeks.

Pre-eruptive: Malaise, fever, lymphadenopathy and mild conjunctivitis. Virus isn’t yet having a huge systemic impact.
Eruptive phase: Symptoms develop to become body wide potentially affecting multiple systems. This includes arthralgia and arthritis if the virus enters the joints, crossing the placenta and damaging the foetus if it occurs in the pregnant woman and finally the skin rash. This usually starts on the face and spreads rapidly to the body. A key difference between Rubella and Measles rashes is that Rubella fades after about 3 days. The rubella rash is usually red, macular and discrete.

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8
Q

TORCH Infection of pregnancy:

A
T: Toxoplasmosis
O: Other
R: Rubella
C: Cytomegalovirus
H: Herpes Simplex Virus – 2

Other diseases:

  • HIV
  • Varicella-Zoster virus (Chicken pox)
  • Hepatitis B
  • Parvovirus B19 (Slapped cheek syndrome)
  • Toxoplasma gondii (Syphilis)
  • Listeria monocytogenes (Listeriosis)
  • Mycobacterium leprae (Leprosy)
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9
Q

Unusual fracture types

A

Pott- a fracture of the distal (situated away from the centre of the body) end of the fibula, with serious injury of the distal tibial articulation
Colles- a fracture in which the distal end of the radius in which the distal fragment is displaced forward
Stress- is a fatigue-induced fracture of the bone caused by repeated stress over time.
Instead of resulting from a single severe impact, stress fractures are the result of accumulated trauma from repeated submaximal loading, such as running or jumping. Because of this mechanism, stress fractures are common overuse injuries in athletes.

Stress fractures can be described as a very small sliver or crack in the bone; and are sometimes referred to as “hairline fractures”.

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10
Q

Lower limb palsies

A

Femoral Nerve dysfunction-
• Weak or unable to flex the hip of extend the knee
• Sensation loss on the anterior and medial aspect of the thigh and the medial side of the leg and foot
Obturator Nerve dysfunction-
• Weak or unable to abduct at the hip
• Sensation loss over the medial aspect of the thigh

Tarsal tunnel syndrome-
This is a condition where the tibial nerve is compressed within the tarsal tunnel (posterior to the medial malleolus). There are varying causes, of which the main three are:
• Osteoarthritis
• Rheumatoid arthritis
• Post-trauma ankle deformities
Patients complain of paraesthesia in the ankle and sole of the foot, which can radiate up the leg slightly. It is aggravated by activity and relieved by rest.
Tarsal tunnel symptoms can be treated conservatively by anti-inflammatory drugs and changes in footwear. If these interventions are not successful, the flexor retinaculum can be cut surgically, which releases the pressure.

Tibial Nerve dysfunction
Damage to the tibial nerve is rare, and is often a result of direct trauma, entrapment through narrow space or compression for long period of time.
• Damage results in loss of plantar flexion, loss of flexion of toes
• Sensation loss on the posterolateral skin surface of the lower leg and all the planter surface of the foot apart from a small section of the medial aspect

Common Fibular Nerve dysfunction-
The common fibular nerve is most commonly damaged by a fracture of the fibula, or the use of a tight plaster cast. The anatomical course of the common fibular nerve causes it to wrap round the neck of the fibular, and so any fractures of the fibular neck can cause nerve palsy.
• Patients with common fibular nerve damage will lose the ability to dorsiflex the foot at the ankle joint. Hence the foot will appear permanently plantar flexed – known as foot drop
Loss of sensation on-
• Lateral aspect of the knee and lower limb
• Dorsal aspect of the foot
• Posteromedial aspect of the planter surface of the foot

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11
Q

Causes of ABG change

A

Causes of metabolic acidosis
• Lactic acidosis: shock, infection, hypoxia.
•Urate (renal failure).
•Ketones (diabetes mellitus, alcohol).
•Diarrhoea.
•Addison’s disease.
•Drugs or toxins: acetazolamide, ammonium chloride.

Causes of metabolic alkalosis
•Vomiting.
•Hypokalaemia - eg, diuretics
•Excessive alkali drugs, such as for acid dyspepsia.
•Burns.

Causes of respiratory acidosis
Acute:
•Depression of the central respiratory centre by cerebrovascular disease or drugs.
•Inability to ventilate adequately due to neuromuscular disease - e.g. myasthenia gravis, amyotrophic lateral sclerosis, Guillain-Barré syndrome, muscular dystrophy.
•Airway obstruction related to asthma or exacerbation of chronic obstructive pulmonary disease (COPD).

Chronic:
•Chronic respiratory acidosis may be secondary to many disorders – e.g. COPD, obesity hypoventilation syndrome

Causes of respiratory alkalosis
Respiratory alkalosis results from hyperventilation - eg, anxiety, stroke, meningitis, altitude, pregnancy

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12
Q

Down’s syndrome Trisomy 21

A

Facial-
•An oval-shaped face.
•Eyes that slant upwards
•A small mouth and a tongue that often protrudes.
•The back of their head (called the occiput) is often flatter than normal.
•Their nose may be small and have a flat and low bridge.
•Ears may also be small and low-set
Other physical features
•Short fingers and a little finger that can curve inwards.
•Muscles that lack tone and can be quite floppy (this is often most noticeable in babies).
•Babies may have a low birth weight.
Mental Retardation
Everyone with Down’s syndrome will have some degree of learning difficulty, however the severity varies from person to person
Other
•90% of patients with Down’s syndrome will have some sort of hearing loss
Around half of babies with Down’s syndrome will have a congenital heart defect, especially atrioventricular septal defect (AVSD).

Women who are at high risk of having a child with downs syndrome are offered diagnostic testing using either chorionic villus sampling (if less than 13 weeks of gestation) or amniocentesis (if beyond 15 weeks of gestation). These procedures carry a risk of miscarriage (0.5-1% excess miscarriage risk for amniocentesis; 1-2% for chorionic villus sampling).

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13
Q

Edwards Syndrome (Trisomy 18)

A

Features
Signs of Edwards’ syndrome include:
•a small, abnormally shaped head
•a small jaw and mouth (micrognathia)
•long fingers that overlap, with short fingernails and clenched fists
•low-set ears
•smooth ‘rocker bottom’ feet (convex bottom of feet)
•heart and kidney problems
•feeding problems in infancy, leading to poor growth
•breathing problems
•hernias
•bone abnormalities, such as a curved spine
•frequent infections of the lungs and urinary system
•a severe learning disability
•New-borns have a 40% chance of surviving to age 1 month.

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14
Q

Patau’s Syndrome (trisomy 13)

A

Features
Many foetuses never survive until term and are stillborn or spontaneously abort.
Signs of Trisomy 13-
•Intrauterine growth restriction and low birth weight.
•Congenital heart defects: these occur in 80%
•Cleft lip and palate.
•Nasal malformation.
•Hypotelorism (reduced distance between the eyes) or cyclops.
•Severe learning disability.
•Problems with control of breathing
•Polydactyly (a condition in which a person or animal has more than five fingers or toes on one, or on each, hand or foot)
•Rocker-bottom feet
•Ear malformations and deafness.
•hernias
Tend to die within days. Maternal age is less influential.

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15
Q

Turners Syndrome 45X

A
•Webbed Neck (KEY SIGN)
•Short Stature
•Normal IQ
•Primary amenorrhoea and Infertility (due to sex hormones oestrogen and progesterone not being produced)
•Broad chest and widely spaced nipples
Patients with Turners syndrome are at an increased risk of chronic condition such as-
•Crohn's disease.
•Coeliac disease.
•Hashimoto's thyroiditis
•Hypertension
•Type 1 diabetes mellitus
•Lymphoedema
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16
Q

Klinefelter’s Syndrome 47XXY

A

Clinical Features
•Infertility
•Small firm testes; decreased facial and pubic hair; loss of libido
•Tall and slender, with long legs, narrow shoulders, and wide hips.
•Gynaecomastia or history of gynaecomastia during puberty; decreased libido; history of undescended testes.
•Learning disability; delayed speech development; behavioural problems; psychosocial disturbances.
•Other features may include tiredness, reduced muscle power and stamina, and truncal obesity
Management
Testosterone replacement
This reduces the risks of most of the long-term complications associated with Klinefelter’s syndrome
•Treatment should begin as they enter puberty.
•XXY males diagnosed in adulthood are also likely to benefit from the hormone.
•A regular schedule of testosterone injections will increase strength and muscle size and promote the growth of facial and body hair.
Prognosis
Increased risk of; breast cancer, osteoporosis, hypothyroidism, diabetes mellitus, etc.
However, overall the lifespan of a male with Klinefelter’s syndrome is normal

•It is the most common sex chromosome disorder, affecting 1 in 660 men

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17
Q

The Abortion Act 1967

A

The Abortion Act 1967 covers England, Scotland and Wales
Normal- 2 Doctors- Before 24 weeks
•abortions must be carried out in a hospital or a specialist licensed clinic
•two doctors must agree that an abortion would cause less damage to a woman’s physical or mental health than continuing with the pregnancy
There are also a number of rarer situations when the law states an abortion may be carried out after 24 weeks. These include:
Emergency- 1 Doctor- Anytime
•if it’s necessary to save the woman’s life
•to prevent grave permanent injury to the physical or mental health of the pregnant woman
Genetic Abnormality- 2 Doctors- Anytime
•if there is substantial risk that the child would be born with serious physical or mental disabilities

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18
Q

Spina Bifida

A

Spina Bifida Occulta: Least severe form. The incomplete fusion is minor and causes very few problems
Meningocele: A cyst pushes through the vertebrae that aren’t fused completely. This cyst contains no nervous tissue, only the meninges*.
Myelomeningocele: A cyst forms through the gap between vertebrae. The cyst contains the spinal cord itself; this is the most severe form with a poor prognosis.

-If a cyst is present the condition is called Spina Bifida Cystica; Meningocele and Myelomeningocele are sub-types of Spina Bifida Cystica.

Myelomeningocele

Raised, red cyst
Have TCS:
Lower limb weakness
Fecal/urinary incontinence
Impaired sensation
Spina Bifida Occulta
Normal, or
Skin Dimple
Tuft of hair 
Usually asymptomatic
Don’t know they have it
Maybe mild back pain

Meningocele

Raised, red cyst
Often asymptomatic
May have tethered spinal cord syndrome
(TCS)

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19
Q

The 3 cardiac shunts

A
  • The Ductus Venousus limits the amount of blood that initially enters the liver instead channeling it towards the Inferior Vena Cava
  • The Foramen Ovale allows most blood to directly enter the left atrium from the right atrium. This allows blood to reach systemic circulation faster.
  • The Ductus Arteriousus allows blood from the pulmonary arteries into the aorta. This reduces the amount of blood going to the lungs and increases the amount of blood available for the brain and rest of the body.
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20
Q

Patent Foramen Ovale

A

Patent Foramen Ovale is associated with strokes, Trans-ischaemic attacks (mini-strokes), Decompression sickness and migraines.

  • Decompression sickness, also called the bends, is where nitrogen gas bubbles form in the venous system. With a PFO these gas bubbles can get into the arterial system and cause occlusions in the systemic circulation.
  • Although strokes and TIA’s can be caused by one of these bubbles if it gets into the brain the main concern with a PFO is from an embolus from a Deep Vein Thrombosis (DVT) crossing into the systemic circulation.
  • DVT’s are clotting in the venous system in the legs, due to a number of factors. These clots occasionally break off and travel to the heart. Normally these go to the lungs and cause a Pulmonary Embolus, but if the patient has a patent foramen ovale then the clot can get into the arterial system. The clot can reach the brain and cause the stroke or TIA.
21
Q

Patent Ductus Arteriousus

A
  • This usually fuses completely after 2-3 weeks after birth.
  • More common in girls than boys (2:1), and affects 1 in 2000 live births.
  • If the PDA remains open then oxygenated arterial blood from the aorta enters the lungs. This puts more strain on the lungs due to volume. There is also less oxygenated blood for the rest of the body.
  • Usually there are no symptoms, but it can cause: Repeat lower respiratory tract infections, increased breathing work and poor weight gain in infants.
  • The key to PDA diagnosis is that a machinery type heart murmur can be heard throughout the whole of the cardiac cycle.
  • To close we give either Ibuprofen or Indomethacin (don’t need to remember these.
22
Q

Pre-eclampsia

A

Pre-eclampsia is pregnancy induced hypertension presenting after 20 weeks associated with significant proteinuria

Pre-eclampsia triad: Hypertension (BP>140/90), Significant protein urea (>0.3g/24h or 20mg/mmol) and facial/limbic oedema. Presence of these 3 after 20 weeks gestation is diagnostic for pre-eclampsia.
-More severe symptoms include: severe headache (often with rapid onset), visual disturbances, epigastric pain (just below ribs), vomiting and sudden onset oedema in face or limbs. Any of these factors in combination with high blood pressure indicates immediate referral to the obstetrics team.
labetalol

23
Q

Raynaud’s phenomenon

A

Raynaud’s phenomenon is caused by vasospasm of small arteries and arterioles that decrease blood flow to the skin.
Raynaud’s phenomenon is fairly common and can be idiopathic (occur on its own) or secondary to other conditions like systemic sclerosis, SLE, RA, Sjogrens, thrombocytosis, polycythaemia rubra vera (PCV).
It is characterised by cold induced colour change of the fingertips white- blue- red and this colour change is well demarcated.

Calcium Channel Blockers (CCBs)
CCBs, usually Nifedipine, are the first-line systemic treatment for Raynaud’s phenomenon. They work because they act as vasodilators, improving blood flow to the digits. It is important to remember that there are other simple interventions that can be taken before trying medications. Smoking cessation is important as smoking has been shown to significantly worsen symptoms. Additionally, encouraging the patient to wear gloves (preferably insulated or self-heating) whenever they are exposed to the cold is important. Other options include ACE inhibitors and IV prostacyclin. In extreme cases nerve blocks or digital amputation might be necessary.

24
Q

Erythema multiforme

A

Erythema multiforme (EM) is a hypersensitivity reaction that in 90% of cases is triggered by infection.

Causes
The commonest infective cause is Herpes simplex virus, but other causes include Mycoplasma, CMV, VZV.

Clinical features
EM minor causes well-defined circular papules on which evolve at different stages to form a ‘target-shaped’ lesion of three concentric rings of different colours. The rash starts on the palms/soles and spread up the limbs to the trunk.

EM major causes a similar rash but also involves at least one mucous membrane, usually the oral mucosa.

Diagnosis
EM is a clinical diagnosis.

Management
Usually no treatment is required as it is self-limiting. The trigger may be treated with anti-virals or antibiotics.

25
Q

Tumour lysis syndrome

A

Tumour lysis syndrome is a common oncological emergency. It is associated with rapid cell death on starting chemotherapy and is common in tumours which are rapidly proliferating. These are classically haematological malignancies such as leukaemia and lymphoma.

Clinical features
It results in an increase in serum urate, potassium and phosphate, precipitating renal failure.

Common symptoms include nausea, vomiting and muscle pain.

Management
Management focuses on preventing this from occurring through giving prophylactic allopurinol and in some cases a recombinant urate oxidase, rasburicase. Good hydration should be maintained.

26
Q

Achalasia

A

Achalasia is a condition of unknown aetiology which causes failure of the lower oesophageal sphincter to relax.

Epidemiology
It is an uncommon condition with an incidence of 1.6 cases per 100,000 individuals. It equally affects men and women. A small percentage of cases are associated with underlying oesophageal cancer.

Presentation of achalasia
Dysphagia – gradual onset (months to years)
Regurgitation of undigested food
Aspiration
Retrosternal chest pain / heartburn – often does not respond to PPI
Weight loss – often mild
Investigations
Endoscopy – may show dilated oesophagus, containing residual material. It also rules out other more sinister pathologies.
Oesophageal manometry – shows high pressure and incomplete lower oesophageal sphincter relaxation
Barium swallow – shows classic ‘bird’s beak appearance’ in advanced disease
Treatments
Medical
Botulinum toxin injections (botox)
Medical therapy can be tried (calcium channel blockers / nitrites) in patients who fail botox therapy or are not suitable surgical candidates
Surgery: Options include oesophageal dilatation and surgical cleavage of the muscle, called ‘Heller’s Myotomy’.
Heller’s cardiomyotomy
This is the correct answer. This patient is displaying signs and symptoms of achalasia, failure of the lower oesophageal sphincter to relax due to degeneration of the myenteric plexus. Patients present with difficulty swallowing both liquids and swallows, in contrast to patients with an obstruction who present with difficulty swallowing solids first. The best treatment for this condition is a Heller’s cardiomyotomy which is a surgical procedure where the muscle fibers of the lower oesophagus are divided.

27
Q

Polyhydroaminos

A

Polyhydramnios is the presence of too much amniotic fluid in the uterus.

Clinical features
Polyhydramnios may present with a uterus which feels tense or large for dates and it may be difficult to feel the foetal parts on palpation of the abdomen. In many cases of polyhydramnios there is no identifiable cause.

Causes
Causes of polyhydramnios can be due to excessive production of amniotic fluid or insufficient removal of amniotic fluid.

Excess production can be due to increased foetal urination:

Maternal diabetes mellitus

Foetal renal disorders

Foetal anaemia

Twin-to-twin transfusion syndrome

Insufficient removal can be due to reduced foetal swallowing:

Oesophageal or duodenal atresia

Diaphragmatic hernia

Anencephaly

Chromosomal disorders

Complications of polyhydramnios
Complications of polyhydramnios can be divided into maternal and foetal.

Maternal complications
Maternal respiratory compromise due to increased pressure on the diaphragm

Increased risk of urinary tract infections due to increased pressure on the urinary system

Worsening of other symptoms associated with pregnancy such as gastro-oesophageal reflux, constipation, peripheral oedema and stretch marks

Increased incidence of caesarean section delivery

Increased risk of amniotic fluid embolism (although this is rare)

Foetal complications
Pre-term labour and delivery

Premature rupture of membranes

Placental abruption

Malpresentation of the foetus (the foetus has more space to “move” within the uterus)

Umbilical cord prolapse (polyhydramnios can prevent the foetus from engaging with the pelvis, thus leaving room for the cord to prolapse out of the uterus before the presenting part)

Management
Treatment includes management of any underlying causes (e.g. in maternal diabetes) and amnio-reduction in severe cases.
Smoking can cause placental insufficiency which can lead to intrauterine growth restriction and oligohydramnios (not polyhydramnios).

28
Q

Ptechial rash

A

A ptechial rash may occur in meningococcal septicaemia. Although meningococcal septicaemia can cause headache, the history of a sudden onset ‘thunderclap’ headache followed by collapse is suggestive of sub-arachnoid haemorrhage

29
Q

Jaundice and ascites +coma

A

Jaundice and ascites occur in decompensated chronic liver disease. Decompensated chronic liver disease may cause hepatic encephalopathy, resulting in a progressive impairment in consciousness. The history of a ‘thunderclap’ headache along with the family history of chronic kidney disease suggests sub-arachnoid haemorrhage secondary to ruptured berry aneurysm, a common association with polycystic kidney disease.

30
Q

Spontaneous upbeat nystagmus +coma

A

Spontaneous upbeat nystagmus may be present in Wernicke’s encephalopathy, a condition caused by vitamin B1 deficiency. Wernicke’s encephalopathy presents with the triad of ataxia, confusion, and oculomotor impairment. The clinical case does not describe any risk factors for vitamin B1 deficiency (such as chronic alcoholism, malnutrition, bariatric surgery, or hyperemesis gravidarum).

31
Q

Bilateral flank masses +coma

A

This is the correct answer. The patient presents with sub-arachnoid haemorrhage secondary to a ruptured berry aneurysm. This is associated with polycystic kidney disease, felt as bilateral flank masses on examination. The family history of chronic kidney disease is consistent with polycystic kidney disease, an autosomal dominant disorder caused by mutation in the PKD1 gene of chromosome 16.

32
Q

Pin-point pupils +coma

A

Pinpoint pupils are indicative of opiate overdose. There are no clues in the question to suggest heroin abuse, such as track marks in the forearms or a history of substance misuse. The history of a sudden onset ‘thunderclap’ headache points towards a sub-arachnoid haemorrhage.

33
Q

Investigation with coma

A

ABCDE Assessment
Blood pressure may be high in hypertensive encephalopathy, or low in hypovolaemic shock.
Core temperature is low in hypothermia.
Examination of the skin may reveal jaundice, suggestive of hepatic encephalopathy, or petechial rash, suggestive of meningococcal sepsis.

Close examination of the head/face should be done to check for signs of a basal skull fracture (with haemotympanum, Battle’s sign, racoon eyes, and CSF rhinorrhoea/otorrhoea).

Glasgow Coma Scale
The Glasgow Coma Scale should be determined to grade the severity of the impairment in consciousness.

Eye response (out of 4.: 4 open spontaneously, 3 open to voice, 2 open to pain, 1 do not open.

Verbal response (out of 5): 5 oriented, 4 confused, 3 inappropriate words, 2 incomprehensible sounds, 1 no sounds.

Motor response (out of 6): 6 obeys command, 5 localises to pain, 4 withdraws to pain, 3 abnormal flexion to pain, 2 extension to pain, 1 no movement.

The threshold for intubation and ventilation is often quoted as GCS of 8 or less (but this can vary according to the clinical situation)

Further Examination in Coma
A focused neurological examination should be carried out to localise the anatomical site of the coma.

It is important to be aware of Cushing’s triad, suggestive of imminent herniation: bradycardia, hypertension, and irregular breathing. This should prompt urgent neurosurgical review.

Oculomotor signs of herniation include: gaze preference to 1 side initially, dilation of the pupil ipsilateral to the lesion (due to stretching of the third cranial nerve), followed by loss of pupillary reactivity due to herniation and midbrain damage.

The pupils can also be helpful in determining the aetiology of the coma - e.g. pinpoint pupils may indicate opiate overdose.

34
Q

Acute pancreatitis - indications and causes

A

Serum lipase
This is the correct answer. This patient is displaying signs and symptoms of acute pancreatitis, which is a common diagnosis in individuals with a history of alcohol excess. A serum lipase will be at least 3 times the upper limit of normal in a diagnosis of pancreatitis, and is specific to this condition.

Bilirubin
This is the incorrect answer. Bilirubin is raised in patients with jaundice, which maybe be caused by a number of conditions including haemolysis, obstruction and acute hepatitis. It will not be diagnostic in this patient.

Gamma GT
This is the incorrect answer. A gamma GT level is likely to be raised in a patient with a history of alcohol excess, but is unlikely to give a diagnosis in this patient, as it is non-specific.

Pancreatitis is a common presentation to the acute surgical take. It is associated with a high morbidity and mortality especially if identified late. It is therefore a critical differential diagnosis for many patients presenting with abdominal pain.

Causes of acute pancreatitis
Causes can be remembered with the mnemonic GET SMASHED:

Gallstones (most common worldwide)
Ethanol (most common cause in Europe)
Trauma
Steroids
Mumps
Autoimmune disease (Polyarteritis Nodosa/SLE)
Scorpion bite (!)
Hypercalcaemia, hypertriglycerideaemia, hypothermia
ERCP
Drugs (as above)
Causes of drug-induced pancreatitis
A good mnemonic for drug-induced pancreatitis is FATSHEEP:
Furosemide
Azathioprine/Asparaginase
Thiazides/Tetracycline
Statins/Sulfonamides/Sodium Valproate
Hydrochlorothiazide
Estrogens
Ethanol
Protease inhibitors and NRTIs
There is some overlap here as some of the drugs listed are sulphonamides.

Thiazides, furosemide, some HIV drugs (protease inhibitors and non-nucleoside reverse transcriptase inhibitors), sulfasalazine and gliclizide are all classed as sulphonamides due to their sulphonamide group.

35
Q

Acute pancreatitis presentation

A

Symptoms
Acute pancreatitis is associated with a stabbing-like, epigastric pain which radiates to the back that is relieved by sitting forward or lying in the fetal position.
Vomiting is highly associated with this.
Importantly, past medical history and social history is vital. A recent alcoholic binge or a history of gallstones are highly suggestive.
Signs
Signs can be variable. Look for symptoms of hypovolaemia (tachycardia, dry mucous membranes due to third-space losses of fluid.
Fever is only present if pancreatitis has been complicated with infection
There may be guarding in the epigastric region, however, these are relatively non-specific signs.
Haemorrhagic pancreatitis although rare shows signs that are Grey-Turner’s sign is known as bruising along the flanks and indicates retroperitoneal bleeding which is highly associated with acute pancreatitis.
Cullen’s sign indicates bruising around the peri-umbilical area which again is highly associated with pancreatitis.
Third space fluid sequestration in pancreatitis is the result of a combination of inflammatory mediators, vasoactive mediators and tissues which lead to vascular injury, vasoconstriction and increased capillary permeability leading to extravasation of fluid into the third space.
This can lead to ARDS (Acute Respiratory Distress Syndrome), pleural effusions and hypovolaemia leading to AKI (Acute Kidney Injury).
Bloods
FBC and Urea and Electrolyes
Leukocytosis can indicate the presence of necrotising pancreatitis.
LFT’s may also be abnormal if there is gallstone disease.
- Lipase is a more sensitive and specific marker than amylase and should be used if available. However, it should be noted that it is often not readily available in UK hospitals
An amylase 3x the upper limit of normal is extremely suggestive of acute pancreatitis.
Importantly, the degree of elevation of amylase is not related to the severity of the disease.
However, other causes such as perforated duodenal ulcer, cholecystitis and mesenteric infarction may also elevate amylase although to a lesser extent.
Imaging investigations
Imaging tests are not useful for the diagnosis of pancreatitis, but may be useful to identify causes.

Ultrasound abdomen can look for gallstones.
MRCP can be used to look for obstructive pancreatitis.
ERCP is often preferred in these cases compared to MRCP and can be therapeutic.
A CT scan can be performed to at a later stage if complications of pancreatitis are suspected such as pseudocysts or necrotizing pancreatitis.
Severity of pancreatitis
The modified Glasgow criteria are used to predict the severity of pancreatitis. In practice this is usually done at admission and after 48 hours of admission. The true score is performed after 48 hours. A score of 3 or more positive factors indicates transfer to ITU/HDU for intensive monitoring and aggressive fluid resuscitation. These indicators are based on the degree of potential complications arising from pancreatitis, such as necrosis of surrounding tissue and therefore saponification, reduced hormone output (insulin) and ARDS.

It can be remembered by the mnemonic PANCREAS:

PaO2 < 8kPa (60mmHg)
Age > 55 years
Neutrophils - WBC >15 x109/l
Calcium < 2mmol/l
Renal function - Urea > 16mmol/l
Enzymes - AST/ALT > 200 iu/L or LDH > 600 iu/L
Albumin < 32g/l
Sugar - Glucose >10mmol/L
36
Q

Management of acute pancreatitis

A

Management
The management of pancreatitis is to help maintain electrolyte imbalances and compensate for the third space losses seen in this disease. Supportive care is the main way of facilitating this –

Aggressive fluid resuscitation with crystalloids

Aim to keep urine output > 30 mL/hour
Start with a 1 litre bolus and try to maintain adequate urine output. This usually amount to a fluid requirement of 3 – 5 ml/kg/hr
Catheterisation

Analgesia

Strong analgesia in the form of opioids are needed
Anti-emetics

IV antibiotics are shown to have no real effect in outcome unless necrotising pancreatitis is present. Necrotising pancreatitis is a complication of severe pancreatitis representing inadequate fluid resuscitation during initial management. It is usually diagnosed by CT scan. Routinely giving antibiotics in pancreatitis is not current clinic practice.

Calcium may be given if hypocalcaemia is present, but is not prescribed prophylactically.

Insulin may also be given in the presence of hyperglycaemia due to the damaged pancreas reducing release of the hormone.

37
Q

Innocent murmurs in children

A

Review again in 2 weeks-
This patient is presenting to the GP with a common cold and a soft systolic murmur at the left sternal edge. This is most likely to be an innocent murmur. Innocent murmurs are very common in children (up to 30% of children at some point), and can be precipitated by febrile illness. As this child currently has a mild viral infection, the best option is to review the murmur in a few weeks once the infection has resolved, to see if the murmur has disappeared with the infection. The infection is likely to be a mild viral upper respiratory tract infection, as evidenced by a lack of tonsillar exudate, angry red throat and no sign of ear infection (bulging tympanic membrane with effusion).

Innocent murmurs are very common benign murmurs that occur in around a third of children at some point during childhood.

Features
The features of ‘innoSent’ murmurs all start with the letter S:

Soft Systolic murmur at the left Sternal edge in an a Symptomatic patient.
Management
Innocent murmurs can be made more prominent when children have a febrile illness. If a murmur like this is discovered when a child has a febrile illness, the best option is to review the child in a few weeks. This will allow assessment of the murmur to see if it has resolved with the infection, in keeping with an innocent murmur. If the murmur persists, then further investigation (e.g. echocardiogram) could be considered.

38
Q

Outflow obstruction urinary retention

A

Complications after relieving outflow obstruction
Differentiating chronic and acute urinary retention
Chronic urinary retention differs from acute urinary retention by the absence of pain or urge to urinate. It has developed over a prolonged period of time.

Differentiating low from high pressure urinary retention
Chronic urinary retention can be differentiated into low or high pressure, by the presence of detrusor activity. Detrusor activity causes high pressure chronic retention which increases the risk of renal damage, high blood pressure and upper renal tract damage.

Complications of relieving urinary retention
Upon relieving urinary obstruction, there’s likely to be a diuresis which is a physiological response to retained sodium, water and urea. Development of post obstructive diuresis occurs when there’s >200ml/hr for 2 consecutive hours.

Management of post obstruction diuresis
Urine osmolarities should be taken as this will determine management.

Iso-osmolar urine indicated the kidneys do not need to concentrate the urine and is consistent with physiological diuresis and it generally self-limiting.
Hyper-osmolarity indicates the kidneys are concentrating urine so post-obstructive diuresis has, or is resolving.
Hypo-osmolarity indicates salt wasting and the inability for the kidneys to concentrate urine. This is pathological and patients should have fluids replaced like for like.

39
Q

Morphine overdose

A

Morphine causes depression of the respiratory centres leading to decreased respiration. This in turn leads to a build up of carbon dioxide (causing acidosis) and reduces oxygenation (causing hypoxia). Morphine also constricts the pupils.

40
Q

Heart failure drugs

A

Furosemide and Spironolactone
First line management in a patient with heart failure and preserved ejection fraction (HFPEF) would be lifestyle advice, low dose diuretic in patients with signs of fluid overload and ACE-inhibitor/ARB if the patient is hypertensive. Furosemide is indicated, however, spironolactone is used in patients with heart failure with reduced ejection fraction (HFPEF) and is a second line treatment option.

5%
Sacubitril/Valsartan
First line management in a patient with heart failure and preserved ejection fraction (HFPEF) would be lifestyle advice, low dose diuretic in patients with signs of fluid overload and ACE- inhibitor/ARB if the patient is hypertensive.

Sacubitril/Valsartan is a relative new heart failure ACE-inhibitor/ARB combination drug but it is indicated in patients with reduced ejection fraction and symptoms corresponding to NYHA II-IV

3%
Furosemide and Bisoprolol
First line management in a patient with heart failure and preserved ejection fraction (HFPEF) would be lifestyle advice, low dose diuretic in patients with signs of fluid overload and ACE- inhibitor/ARB if the patient is hypertensive. Furosemide is indicated, however, beta blockers used in patients with heart failure with reduced ejection fraction (HFPEF). Bisoprolol would also be a relative contraindication given his history of asthma.

12%
Furosemide and Rampril
This is the correct answer. First line management in a patient with heart failure and preserved ejection fraction (HFPEF) would be lifestyle advice for risk factor reduction, low dose diuretic in patients with signs of fluid overload and ACE- inhibitor/ARB if the patient is hypertensive.

61%
Ramipril and Spironolactone
First line management in a patient with heart failure and preserved ejection fraction (HFPEF) would be lifestyle advice, low dose diuretic in patients with signs of fluid overload and ACE- inhibitor/ARB if the patient is hypertensive. Ramipril is indicated, however, spironolactone is used in patients with heart failure with reduced ejection fraction (HFPEF) and is a second line treatment option.

Causes of systolic heart failure
Ischaemic heart disease
Dilated cardiomyopathy
Myocarditis
Infiltration (e.g. in haemochromatosis or sarcoidosis)
Causes of diastolic heart failure
Hypertrophic obstructive cardiomyopathy
Restrictive cardiomyopathy
Cardiac tamponade
Constrictive pericarditis
High output cardiac failure definition
Heart failure is defined as failure of the heart to generate sufficient cardiac output to meet the metabolic demands of the body.

In high output cardiac failure cardiac output is normal, but there is an increase in peripheral metabolic demands which exceed those that can be met with maximal cardiac output.

Causes of high output cardiac failure
Causes of high output cardiac failure can be remembered by the mnemonic AAPPTT:

Anaemia
Arteriovenous malformation
Paget's disease
Pregnancy
Thyrotoxicosis
Thiamine deficiency (wet Beri-Beri)
Clinical features of left heart failure
Left heart failure causes pulmonary congestion (pressure builds up behind the left heart i.e. in the lungs) and systemic hypoperfusion (reduced left heart output).

NB: Sometimes left sided heart failure can lead to pulmonary congestion which in turn also pushes the right ventricle into failure. In these cases signs and symptoms of both left and right sided heart failure may be present.

Symptoms caused by pulmonary congestion
Shortness of breath on exertion
Orthopnoea
Paroxysmal nocturnal dyspnoea
Nocturnal cough (± pink frothy sputum)
Signs caused by pulmonary congestion
Tachypnoea
Bibasal fine crackles on auscultation of the lungs
Signs caused by systemic hypoperfusion
Cyanosis
Prolonged capillary refill time
Hypotension
Less common signs of left heart failure
Pulsus alternans (an alternating strong and weak pulse)
S3 gallop rhythm (due to filling of a stiffened ventricle)
Features of functional mitral regurgitation
Clinical features of right heart failure
Right heart failure causes venous congestion (pressure builds up behind the right heart) and pulmonary hypoperfusion (reduced right heart output).

Symptoms caused by venous congestion
Ankle swelling
Weight gain
Abdominal distension and discomfort,
Anorexia/nausea.
Signs caused by venous congestion
Raised JVP
Pitting ankle/sacral oedema
Tender smooth hepatomegaly
Ascites
Transudative pleural effusions (typically bilateral)
New York Heart Association Classification of Heart failure
The NYHA Classification system is used to classify severity of cardiovascular disability through severity of exertional dyspnoea limiting activity, or discomfort at rest. It runs from Class I (no limitation) to Class IV (discomfort at rest).

Class I - no limitation in physical activity, and activity does not cause undue fatigue, palpitation or dyspnoea.
Class II - slight limitation of physical activity, and comfort at rest. Ordinary physical activity causes fatigue, palpitation and/or dyspnoea.
Class III - marked limitation in physical activity, but comfort at rest. Minimal physical activity causes fatigue (less than ordinary).
Class IV - inability to carry on any physical activity without discomfort, with symptoms occurring at rest. If any activity takes place, discomfort increases.
Investigations in heart failure
Investigations depends on the presentation of the patient.
In a patient presenting to the general practitioner with suspected heart failure investigations should be carried out as follows:

ECG features
This may be normal or reveal clues as to the underlying cause of the heart failure (e.g. ischaemic changes or arrhythmias).

NT-proBNP interpretation
BNP is released by the ventricles in response to myocardial stretch.

BNP has a high negative predictive value, so if the BNP is not raised the diagnosis of congestive cardiac failure is highly unlikely.

If the BNP is raised, the patient should be referred for trans-thoracic echocardiogram.

If BNP>2000ng/L the patient needs an urgent 2 week referral for specialist assessment and an ECHO.
If BNP 400-2000ng/L the patient should get a 6 week referral for specialist assessment and an ECHO.
Echocardiogram interpretation
Echocardiogram will confirm the presence and degree of ventricular dysfunction.

Ventricular dysfunction is normally measured by the ejection fraction.
<40% = heart failure is reduced ejection fraction
Greater than 40% but raised BNP = Heart failure with preserved ejection fraction
Blood tests
U+Es to assess renal function (for medication) and to look for hyponatraemia
LFTs for hepatic congestion
TFTs to check for hyperthyroidism
Glucose and lipid profile to assess modifiable cardiovascular risk factors
BNP is significantly associated with a diagnosis of heart failuare
Chest Xray findings
Chest x-ray findings in heart failure can be remembered by the ABCDEF mnemonic:
A: Alveolar oedema (with ‘batwing’ perihilar shadowing)
B: Kerley B lines (caused by interstitial oedema)
C: Cardiomegaly (cardiothoracic ratio >0.5)
D: upper lobe blood diversion
E: Pleural effusions (typically bilateral transudates)
F: Fluid in the horizontal fissure
Lifestyle modification
Smoking cessation
Salt and fluid restriction (this improves mortality)
Supervised cardiac rehabilitation
Pharmacological management
ACE-inhibitor and beta-blocker (these improve mortality)
Consider angiotensin receptor blocker (ARB) if intolerant to ACE inhibitors
Consider hydralazine and a nitrate intolerant to ACE-I and ARB.
Loop diuretics such as furosemide or bumetanide improve symptoms (but NOT mortality)
If symptoms persist and NYHA Class 3 or 4 consider:
Aldosterone antagonists such as spironolactone or eplerenone. These drugs also improve mortality.
Hydralazine and a nitrate for Afro-Caribbean patients
Ivabradine if in sinus rhythm and impaired ejection fraction
Angiotensin receptor blocker
Digoxin - useful in those with AF. This worsens mortality but improves morbidity.
Surgical/device management options
Cardiac resynchronisation therapy
ICDs are indicated if the following criteria are fulfilled:
QRS interval <120ms, high risk sudden cardiac death, NYHA class I-III
QRS interval 120-149ms without LBBB, NYHA class I-III
QRS interval 120-149ms with LBBB, NYHA class I
Initial Management of acute heart failure (pulmonary oedema)
Sit the patient up
Oxygen therapy (aiming saturations >94% in normal circumstances)
IV furosemide 40mg or more (with further doses as necessary) and close fluid balance (aiming for a negative balance)
SC morphine - this is contentious with some studies suggesting that it might increase mortality by suppressing respiration
Advanced management of acute heart failure (pulmonary oedema)
The following usually occurs in a high dependency or ITU setting.

CPAP - reduces hypoxia and may help push fluid out of alveoli
Intubation and ventilation
Furosemide infusion - continuous IV furosemide given over 24 hours to maximise diuresis
Dopamine infusion - Continuous IV dopamine given over 24 hours. It works by inhibiting sympathetic drive and thereby increasing myocardial contractility.
Intra-aortic balloon pump - if the patient is in cardiogenic shock
Ultrafiltration - If resistant to or contraindicated diuretics
Note that GTN infusion is no longer routinely used in acute heart failure

Adverse effects of heart failure medications
Common adverse effects for different medications are listed below

Beta blockers: Bradycardia, hypotension, fatigue, dizziness
ACE inhibitors: Hyperkalaemia, renal impairment, dry cough, lightheadedness, fatigue, GI disturbances, angioedema
Spironolactone: Hyperkalaemia, renal impairment, gynaecomastia, breast tenderness/hair growth in women, changes in libido
Furosemide: Hypotension, hypoatraemia/kalaemia,
Hydralazine/nitrate: Headache, palpitation, flushing
Digoxin: Dizziness, blurred vision, GI disturbances

41
Q

Hyperuricaemia

A

Hyperuricaemia may be caused by increased urate production or impaired urate excretion.

Causes
Increased production

Tumour lysis (particularly lymphoma and leukaemia)
Haemolysis
Psoriasis
Rhabdomyolysis
Decreased excretion
Primary gout
Chronic kidney disease
Thiazides
Loop diuretics
Other causes

Hypertension
Hyperlipidaemia

42
Q

Back pain causes

A

Features of ankylosing spondylitis back pain
Prolonged morning stiffness.

Improved with Movement.

Alternating buttock pain.

Features of bone metastasis / myeloma back pain
History of cancer.

Systemic cancer symptoms eg. fever / weight loss / night sweats.

Features of discitis back pain
Systemic infection symptoms eg. fever / weight loss / night sweats.

Immunosuppression.

IV drug usage.

Features of vertebral fracture back pain
Violent trauma.
Features of cauda equina syndrome / spinal cord compression back pain
New urinary or faecal retention or incontinence

Poor anal tone or reduced perineal sensation (saddle anaesthesia)

Bilateral lower limb neurology (alternating or simultaneous)

Features of nerve root compression back pain
Normally unilateral (unless there is bilateral disease)

Burning/shooting pain down the leg

Positive sciatic stretch test

Dermatomal stretch test positive

Reduced reflexes

Cancers that metastasise to the bone
Cancers that commonly metastasise to the bone can be remembered with the mnemonic BLT with a Kosher Pickle:

Breast
Lung
Thyroid
Kidney
Prostate.
43
Q

Guillain barre

A

GBS is an ascending inflammatory demyelinating polyneuropathy.

Causes
Typically 1-3 weeks after infection (e.g. Campylobacter, mycoplasma, EBV). 40% of cases are idiopathic.

Clinical features
Progressive ascending symmetrical limb weakness (affecting the lower limbs first). Paraesthesiae may precede the onset of motor symptoms. Respiratory muscles may be affected in severe cases. Some cases present with symptoms of cranial nerve palsies (e.g. diplopia, facial droop).

Lower motor neurone signs in the lower limbs (hypotonia, flaccid paralysis, areflexia). Cranial nerve signs may also be present (e.g. ophthalmoplegia, lower motor neurone facial nerve palsy, bulbar palsy) as well as signs of type 2 respiratory failure due to respiratory muscle weakness (e.g. CO2 flap, bounding pulse). Autonomic dysfunction may be present (e.g. arrhythmia, labile blood pressure).

Investigations
Bedside tests include spirometry (checking for a reduced FVC). Bloods include an ABG (to check for type 2 respiratory failure) and anti-ganglioside antibodies. Other investigations include a lumbar puncture which typically shows a raised protein, with normal cell counts and glucose (so called albuminocytological dissociation).

Management
Conservative measures include monitoring of ventilation (with serial spirometry and ABG) ± ventilation, measures to reduce the risk of VTE (TEDs, LMWH), and protection of pressure areas. Medical management is with intravenous immunoglobulin and, if ineffective, plasmapheresis.

Note that Miller-Fisher syndrome (a variant of GBS) presents with ataxia, ophthalmoplegia, and areflexia. The condition is typically positive for anti-GQ1b antibodies.

44
Q

Causes of hearing loss

A

rescbyacusis
Prescbyacusis describes age-related hearing loss. Her young age makes this diagnosis unlikely. Additionally, presbyacusis describes a sensorineural hearing loss, which would be worse with background noise, not better.

6%
Otosclerosis
This patient has risk factors for otosclerosis: onset in early adulthood, exacerbated by pregnancy. Otosclerosis is usually bilateral and causes a conductive deafness (better with background noise). It is frequently associated with tinnitus (high pitched ringing noise). The otoscopy image clinches the diagnosis - this patient has a pink tinge to the tympanic membrane, which is known as Schwarze sign or Flamingo flush, which only occurs in 10% otosclerosis cases but is highly specific.

64%
Vestibular schwannoma
This is more likely to cause a sensorineural hearing loss (worse in background noise) than conductive. It very rarely occurs bilaterally. Indeed, bilateral schwannoma should prompt consideration of a genetic syndrome e.g. neurofibromatosis. It is not associated with pregnancy.
Otosclerosis is the most common cause of progressive deafness in young adults.

45
Q

Otosclerosis

A

Inheritance
It is an autosomal dominant condition and the majority of patients have significant family histories.

Pathophysiology
In otosclerosis, the bone around the base of the stapes becomes thickened and eventually fuses with the bone of the cochlea.
This prevents the stapes natural function as a piston onto the cochlea and conduction progressively gets worse until a maximal conductive hearing loss of 60dB is reached.
Management
Initial treatment for otosclerosis may involve hearing amplification through hearing aids or surgical replacement of the stapes bone through a stapedectomy

46
Q

Nephrotic syndrome

A

Nephrotic syndrome is a clinical syndrome that arises secondary to increased permeability of serum protein through a damaged basement membrane in the renal glomerulus.

Clinical Features
It is typically characterised by a proteinuria (>3-3.5g/day), oedema, hypoalbuminaemia and hyperlipidaemia and lipiduria.

Pathophysiology
Cytokines damage podocytes causing them to fuse together and destroy charge of the glomerular basement membrane.
This allows increased permeability to plasma proteins. This causes massive protein loss in the urine.
As a result of this, serum albumin levels are reduced beyond the synthetic ability of the liver.
Thus patients experience marked oedema as with less albumin in the blood stream, there is less oncotic pressure.
This lets fluid leak out into the interstitium.
As an attempt to maintain oncotic pressure, the liver tries to compensate by increased synthesis of lipoproteins, this is one of the mechanisms postulated to cause the hyperlipidaemia.
However, the full mechanism is not fully understood.
Causes
The most common cause in adults is membraneous glomerulonephritis. The most common cause in children is minimal change disease.

Systemic Disease
Diabetes Mellitus (Glomerulosclerosis)
Systemic Lupus Erythematosus (Membranous)
Amyloidosis
Minimal Change Glomerulonephritis
Associated with upper respiratory tract infection
Biospy: normal light microscopy, fusion of podocytes on electron microscope
Treat with steroids
1% go on to have end-stage renal failure
Membranous nephropathy
Associated with cancers (Lung, Colon Breast), infections (SLE, thyroid disease), infections (Hepatitis B) and drugs (Penicillamine and Gold)
Biopsy: subepithelial immune complex deposits
40% have spontaneous remission
Focal segmental glomerulosclerosis
More common in Afro-caribbean population
Associated with Berger’s disease, sickle cell, HIV
Biopsy: focal scarring, IgM deposition
Treat with steroids or cylophosphamide/ciclosporin
30-50% progress to end stage renal failure
Membranoproliferative/Mesangiocapillary
Less common
May present as both nephrotic or nephritic
Associated with Hepatitis B, Hepatitis C and Endocarditis
50% progress to End-Stage Renal Failure
Clinical Presentation
Periorbital and peripheral oedema.

Investigations
Bedside investigation include urine dipstick which reveals proteinuria. Urine analysis reveals a raised albumin creatinine ratio.
Renal biopsy is indicated in all adults but should only be done in children with an atypical presentation (e.g. steroid unresponsive, haematuria, under 1 years old or over 12 years old).
Management
High dose steroids which should be tapered according to clinical response.
Complications
Infection (due to urinary loss of immunoglobulins)
Venous thromboembolism (due to urinary loss of antithrombin III)
Hyperlipidaemia (due to increased hepatic production of lipids to restore the serum oncotic pressure)
Prescribe a long-course of Prednisolone
This is the correct answer. This patient has presented with clinical features of nephrotic syndrome including significant peripheral oedema and massive proteinuria. This is due to minimal change glomerulonephritis, the most common cause of nephrotic syndrome in children. The disease is caused by effacement of glomerular podocyte processes, which can only be detected using high resolution electron microscopy. No glomerular abnormalities are typically visualised using light microscopy, giving the disease its name. The definitive management of minimal change glomerulonephritis at initial presentation is with a 12-week course of Prednisolone.

Albumin infusion, fluid restriction and advise low salt diet
Fluid restriction and a low salt diet are conservative measures in the management of nephrotic syndrome, but would not be effective at addressing minimal change glomerulonephritis, which is the underlying cause for this patient’s presentation. An Albumin infusion would be appropriate in patients with nephrotic syndrome who present with significant respiratory distress, haemodynamic instability, and significant oedema. However, this patient’s observations are stable.

47
Q

Tuberculosis (TB)

A

Tuberculosis (TB) is a chronic granulomatous disease caused by Mycobacterium tuberculosis.

Transmission
Tuberculosis is transmitted by inhalation of droplets infected with Mycobacterium tuberculosis. These droplets are produced by infected patients when they cough, and infective organisms can survive for long periods of time in the environment.

Epidemiology
1/3 of the global population has latent TB infection
More than 95% of deaths due to TB occur in low and middle-income countries, where it is a leading cause of more mortality
1/5 of all HIV deaths are due to TB.
The incidence of TB in the UK is high compared to other Western countries (13.9/100000 in 2012).
Clinical Features
Primary and secondary infection:

In 90% the immune system contains the infection, through macrophages that engulf bacteria and localize them to the hilar lymph nodes. Here, they are eliminated or may be encapsulated by a barrier of granulation tissue (considered to be in a dormant state).
A small proportion progress to active TB, with an increased risk in those who are immunosuppressed (e.g. HIV). This is known as Secondary TB and usually occurs in the apex of the lungs. From here it can spread locally or to distant sites.
Some patients are not able to contain the primary infection, and it disseminates widely via the bloodstream. This is known as miliary TB (due to the characteristic pattern on Chest X-ray like ‘millet-seeds’ when re-infection of lungs occurs after passing through circulation).
Risk Factors
Ethnic minority groups (most commonly those from sub-Saharan Africa and South Asia). The risk is highest if returned from a high-prevalence country in the last 5 years.
The homeless - associated with overcrowding, poor living conditions and malnutrition.
Drug and alcohol abuse - associated with overcrowding, poor living conditions, and malnutrition.
Close contact with infected patient: household members have a 1/3 risk of infection. However, healthcare workers, and contacts at school or work are also at particular risk.
Immunosuppression: result in reactivation of latent disease or primary miliary infection. Conditions include HIV, chronic organ failure, Diabetes Mellitus, chronic malnutrition.
Young or old age: due to immature immune systems in the very young.
General Presentation
Subacute to chronic in onset
Symptoms depend on the main site of infection, but are usually accompanied by;
night sweats
fever
weight loss
other systemic symptoms
Pulmonary Presentation
Most common
Chronic cough productive of purulent sputum +/- hemoptysis.
Can get bronchiectasis, pneumonia and pleural effusions.
CNS Presentation
TB meningitis or tuberculoma
Headache
Meningism
Focal neurological signs
Decreased consciousness
Genitourinary Presentation
Second most affected organ system outside of the lungs.
Causes ‘sterile’ pyuria, kidney pathology, abscesses, salpingitis and infertility, epididymo-orchitis.
Musculoskeletal Presentation
Arthritis
Osteomyelitis
Psoas abscess
Pott’s Disease of the Spine.
Gastrointestinal Presentation
Abdo pain
Obstruction, appendicitis due to ileocaecal lesions. Can get spread to peritoneum causing ascites.
Pericardial Presentation
Pericardial effusions
Constrictive pericarditis (usually see calcification of the pericardium on imaging)
Lymph Nodes
May get palpable tender, firm superficial lymphadenopathy.
These can later become suppurative (known as scrofuloderma)
Cutaneous Presentation
A wide range of skin reactions including erythema nodosum and Bazin’s disease.
Investigations
Chest X-ray
Sputum samples for culture and sensitivity testing (at least three needed - may need to consider lavage or sputum induction if cannot produce)
Samples from non-pulmonary sites: may need biopsy and needle aspiration
Samples are stained with Ziehl-Neelsen or Auramine staining for direct microscopy
For culture, Lowenstein-Jensen (LJ) media is needed.
PCR - GeneXpert, rapid results with additional drug sensitivity tested as well.
Interferon-Gamma Release Assays (IGRAs) - cannot tell difference between latent or active TB, and not useful in very young or immunosuppressed patients. Results are obtained rapidly, however, and are not affected by prior BCG.
Mantoux test - usually offered to contacts of infected patients. Positive in those who have had the BCG vaccine.
Management
Isoniazid, rifampicin, ethambutol, and pyrazinamide for 2 months, then Isoniazid and rifampicin for a further 6 months.
Extended duration in TB meningitis, pericarditis, and spinal TB.
Side effects of Isoniazid
Peripheral neuropathy (pyridoxine is given to prevent this)
Liver toxicity
Side effects of Rifampicin
Liver toxicity
Hepatic enzyme (p450) inducer
Turns bodily fluids red/orange color.
Side effects of Ethambutol
Visual disturbance (color blindness, loss of acuity etc.)
Avoid in chronic kidney disease.
Side effects of Pyrazinamide
Liver toxicity
Second line treatments
Note that MDR-TB and extensively drug-resistant TB are increasing in global incidence, particularly in South Africa, Eastern Europe, and Asia. Second-line drugs for MDR-TB include amikacin, macrolides, quinolones, and capreomycin. Extensively drug-resistant TB is very difficult to treat, particularly in low-resource countries.

Start initial phase quadruple antibiotic therapy immediately
It is important to start therapy without delay when signs and symptoms point to a diagnosis of acute pulmonary TB. According to both British Thoracic Society and NICE guidelines, you can start treatment without waiting for the results of the sputum culture (which you would ideally ask the patient to produce prior to starting therapy).
The classic quadruple therapy regimen includes Isoniazid, Rifampicin, Ethambutol and Pyrazinamide.

48
Q

Vertigo and Dizziness

A

Vertigo is a hallucination of movement of oneself or one’s surroundings. This movement is often rotatory; for example, one may feel as though the floor is tilting.

Causes of vertigo
There are several causes of vertigo:

Benign positional paroxysmal vertigo (BPPV) features
The presence of debris in the semicircular canals of the ears causes vertigo upon head movement.
The Hallpike manoeuvre is diagnostic, where certain movements of the head causes fatiguable nystagmus.
Epley manoeuvres treat BPPV by clearing the debris.
Acute labyrinthitis features
Inflammation of the vestibular nerve causes an acute severe vertigo, which may be associated with vomiting.
The term ‘vestibular neuritis’ is sometimes used interchangeably but should be confined to cases where only the vestibular nerve is involved. In practice, acute labrynthitis and vestibular neuritis can be distinguished by the presence and absence of hearing dysfunction.
Therefore, acute labrynthitis can present with hearing loss and tinnitus, whereas vestibular neuritis does not.
It is often associated with a recent viral illness or a vascular lesion, in which case it may involve other cranial nerve deficits.
It often resolves completely over a month, so treatment is conservative, although sedatives may help in severe cases.
Ménière’s disease features
Endolymphatic system pressure increases causes recurrent episodes of vertigo, sensorineural hearing loss, tinnitus, and a feeling of aural fullness.
Treatment involves antihistamines and bed rest.
Acoustic neuroma features
Actually a vestibular schwannoma.
They usually present with unilateral hearing loss and progress to involve cranial nerves 5, 6, 9, 10, and the ipsilateral cerebellum.
Ramsay Hunt syndrome features
Herpetic infection of the facial nerve causes a facial nerve palsy, with or without vertigo, tinnitus, and hearing loss.
This is treated with aciclovir and prednisolone.
Ototoxicity features
Caused by aminoglycoside antibiotics (eg. gentamicin, vancomycin) and loop diuretics (eg. furosemide), most commonly

49
Q

Obstructive sleep apnoea

A

Obstructive sleep apnoea is caused by intermittent closure and collapse of the upper airway leading to apnoeic episodes during sleep.

Presentation
Excessive daytime sleepiness
Lack of concentration
Snoring
Unrefreshing sleep
Irritability/personality change
Risk factors
Obesity
Male
Smoking
Alcohol excess
Micrognathia
Neuromuscular disease
Investigations
Polysomnography is the traditional gold standard investigation. Physiological parameters are measured while the patient is asleep overnight
Blood pressure
Management
Weight loss
Smoking cessation
Alcohol avoidance in the evening (sedative effect)
CPAP (Continuous positive airway pressure) maintains upper airway patency and is the gold standard
Complications
Accidents related to excessive daytime sleepiness
Cardiovascular complications such as hypertension
Psychological consequences
Association with other cardiovascular comorbidities such as coronary artery disease, myocardial infarction, stroke and type 2 diabetes
Associated with increase in all cause mortality