AKT 3 Flashcards

1
Q

What is a common side effect of Methotrexate?

A

Myelosuppression

Other side effects include liver cirrhosis and pneumonitis.

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2
Q

What side effect is associated with Sulfasalazine?

A

Rashes

Additional side effects include oligospermia, Heinz body anaemia, and interstitial lung disease.

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3
Q

What is a side effect of Leflunomide?

A

Liver impairment

Other effects include interstitial lung disease and hypertension.

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4
Q

What side effect is linked to Hydroxychloroquine?

A

Retinopathy

Another side effect is corneal deposits.

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5
Q

Which side effect is associated with Prednisolone?

A

Cushingoid features

Additional side effects include osteoporosis, impaired glucose tolerance, hypertension, and cataracts.

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6
Q

What is a side effect of Gold treatment?

A

Proteinuria

This is a notable side effect of gold therapy.

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7
Q

What side effect is associated with Penicillamine?

A

Proteinuria

It can also exacerbate myasthenia gravis.

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8
Q

What side effect is linked to Etanercept?

A

Demyelination

It may also reactivate tuberculosis.

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9
Q

What is a potential side effect of Infliximab?

A

Reactivation of tuberculosis

It is a significant risk associated with this treatment.

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10
Q

What side effect is associated with Adalimumab?

A

Reactivation of tuberculosis

Similar to Infliximab, this is a notable risk.

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11
Q

What common issue occurs with Rituximab treatment?

A

Infusion reactions are common

This is a frequently observed side effect.

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12
Q

What side effect can NSAIDs like naproxen and ibuprofen cause in asthmatics?

A

Bronchospasm

Other side effects include dyspepsia and peptic ulceration.

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13
Q

What is travellers’ diarrhoea?

A

At least 3 loose to watery stools in 24 hours with or without abdominal cramps, fever, nausea, vomiting or blood in the stool

The most common cause is Escherichia coli.

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14
Q

What is the most common cause of travellers’ diarrhoea?

A

Escherichia coli

This bacterium is frequently associated with gastrointestinal infections in travelers.

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15
Q

What characterizes acute food poisoning?

A

Sudden onset of nausea, vomiting and diarrhoea after ingestion of a toxin

Commonly caused by Staphylococcus aureus, Bacillus cereus, or Clostridium perfringens.

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16
Q

Which bacterium is commonly associated with severe vomiting and a short incubation period?

A

Staphylococcus aureus

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17
Q

What are the symptoms of giardiasis?

A

Prolonged, non-bloody diarrhoea

Treatment is with metronidazole.

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18
Q

What is a hallmark symptom of cholera?

A

Profuse, watery diarrhoea

It can lead to severe dehydration and weight loss.

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19
Q

What type of diarrhoea is associated with Shigella?

A

Bloody diarrhoea

Accompanied by vomiting and abdominal pain.

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20
Q

What is a common complication of Campylobacter infection?

A

Guillain-Barré syndrome

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21
Q

What are the two types of illnesses caused by Bacillus cereus?

A
  1. Vomiting within 6 hours, typically due to rice
  2. Diarrhoeal illness occurring after 6 hours
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22
Q

What describes the onset of amoebiasis?

A

Gradual onset bloody diarrhoea, abdominal pain and tenderness lasting several weeks

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23
Q

List the causes of bloody diarrhoea.

A
  • Campylobacter (occasionally)
  • Shigella
  • Amoebiasis (gradual onset)
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24
Q

What is the incubation period for Staphylococcus aureus?

A

1-6 hours

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25
Q

What is the incubation period for Salmonella and Escherichia coli?

A

12-48 hours

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26
Q

What is the incubation period for Shigella and Campylobacter?

A

48-72 hours

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27
Q

What is the incubation period for Giardiasis and Amoebiasis?

A

> 7 days

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28
Q

What is a Fibroadenoma?

A

Common in women under the age of 30 years, described as ‘breast mice’ due to being discrete, non-tender, highly mobile lumps

Fibroadenomas are benign breast tumors that are often found in young women.

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29
Q

What is Fibroadenosis also known as?

A

Fibrocystic disease, benign mammary dysplasia

This condition is characterized by ‘lumpy’ breasts which may be painful, with symptoms worsening prior to menstruation.

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30
Q

What are the characteristic features of breast cancer?

A

Hard, irregular lump; may have associated nipple inversion or skin tethering

Early detection is crucial for better outcomes in breast cancer treatment.

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31
Q

What is Paget’s disease of the breast?

A

Intraductal carcinoma associated with reddening and thickening of the nipple/areola, resembling eczematous changes

This condition can indicate underlying breast cancer.

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32
Q

What is Mammary duct ectasia?

A

Dilatation of the large breast ducts, most common around menopause

May present with a tender lump around the areola and green nipple discharge; if ruptured, can cause local inflammation.

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33
Q

What is a Duct papilloma?

A

Local areas of epithelial proliferation in large mammary ducts, hyperplastic lesions rather than malignant or premalignant

May present with blood-stained discharge.

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34
Q

What is Fat necrosis?

A

More common in obese women with large breasts; may follow trivial trauma, presenting as a firm round lesion but may develop into a hard irregular lump

This condition is rare and can mimic breast cancer, warranting further investigation.

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35
Q

What is a Breast abscess?

A

More common in lactating women; characterized by red, hot tender swelling

Prompt treatment is necessary to manage abscesses effectively.

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36
Q

Fill in the blank: Lipomas and _______ may also develop around the breast tissue.

A

sebaceous cysts

These are generally benign conditions that can occur in breast tissue.

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37
Q

What is required for patients taking antipsychotic medication?

A

Extensive monitoring in addition to clinical follow-up

The monitoring includes various health factors that need to be measured regularly.

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38
Q

What factors need to be measured when on antipsychotics?

A
  • Full blood count (FBC)
  • Urea and electrolytes (U&E)
  • Liver function tests (LFT)
  • Lipids
  • Fasting glucose
  • Prolactin
  • Weight
  • Blood pressure
  • ECG
  • Qrisk/cardiovascular assessment

These factors are critical for ensuring the safety and effectiveness of antipsychotic treatment.

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39
Q

When should FBC, U&E, and LFT be measured for antipsychotic therapy?

A

At the start of therapy and annually

These tests are crucial for monitoring potential side effects of antipsychotic medications.

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40
Q

How often does clozapine require monitoring of FBC?

A

Initially weekly

Clozapine has a higher risk of agranulocytosis, necessitating more frequent monitoring.

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41
Q

When should lipids and weight be measured during antipsychotic therapy?

A

At the start of therapy, at 3 months, and annually

Monitoring these factors helps assess metabolic side effects of antipsychotics.

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42
Q

When should fasting blood glucose and prolactin be measured?

A

At the start of therapy, at 6 months, and annually

This monitoring is important to detect metabolic changes and hormonal effects.

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43
Q

When should blood pressure be monitored during antipsychotic therapy?

A

Baseline and frequently during dose titration

Blood pressure monitoring is essential to manage potential cardiovascular risks.

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44
Q

When should an electrocardiogram (ECG) be performed?

A

At baseline

An ECG helps identify any pre-existing cardiac issues before starting treatment.

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45
Q

How often should cardiovascular risk assessment be conducted?

A

Annually

This assessment is crucial for patients on antipsychotics to manage long-term health risks.

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46
Q

When should clozapine be introduced in the treatment of schizophrenia?

A

If schizophrenia is not controlled despite the sequential use of two or more antipsychotic drugs, one of which should be a second-generation antipsychotic drug, each for at least 6-8 weeks.

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47
Q

What is the incidence of agranulocytosis with clozapine?

A

1%

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48
Q

What is the incidence of neutropaenia with clozapine?

A

3%

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49
Q

What effect does clozapine have on seizure threshold?

A

It can reduce seizure threshold and induce seizures in up to 3% of patients.

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50
Q

List some adverse effects of clozapine.

A
  • Agranulocytosis
  • Neutropaenia
  • Reduced seizure threshold
  • Constipation
  • Myocarditis
  • Hypersalivation
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51
Q

What should be done before starting treatment with clozapine?

A

A baseline ECG should be taken.

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52
Q

What might necessitate a dose adjustment of clozapine?

A

If smoking is started or stopped during treatment.

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53
Q

What is lithium used for in psychiatric treatment?

A

Prophylaxis in bipolar disorder and adjunct in refractory depression

Lithium is primarily used to stabilize mood in bipolar disorder patients and can also help those with treatment-resistant depression.

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54
Q

What is the therapeutic range for lithium?

A

0.4-1.0 mmol/L

This narrow therapeutic range means careful monitoring is essential to avoid toxicity.

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55
Q

What is the primary route of excretion for lithium?

A

Kidneys

Lithium is primarily excreted unchanged in the urine, necessitating renal function monitoring.

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56
Q

What are the two theories regarding lithium’s mechanism of action?

A
  • Interferes with inositol triphosphate formation
  • Interferes with cAMP formation

The exact mechanism remains unclear, but these theories suggest how lithium may influence neurotransmitter signaling.

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57
Q

List some common adverse effects of lithium.

A
  • Nausea/vomiting
  • Diarrhoea
  • Fine tremor
  • Nephrotoxicity
  • Thyroid enlargement
  • ECG changes
  • Weight gain
  • Idiopathic intracranial hypertension
  • Leucocytosis
  • Hyperparathyroidism

These adverse effects require monitoring and may necessitate adjustments in treatment.

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58
Q

What is a specific renal adverse effect associated with lithium?

A

Nephrogenic diabetes insipidus

This condition leads to polyuria and can significantly affect fluid balance.

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59
Q

When should lithium levels be checked after starting therapy?

A

Weekly and after each dose change until stable

Regular monitoring is crucial to ensure therapeutic effectiveness and safety.

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60
Q

How often should lithium blood levels be checked once established?

A

Every 3 months

Consistent monitoring helps prevent toxicity and manage therapeutic levels.

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61
Q

What additional monitoring is required for patients on lithium?

A
  • Thyroid function every 6 months
  • Renal function every 6 months

Due to the potential for thyroid and renal adverse effects, regular assessments are necessary.

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62
Q

What patient education materials should be provided to those on lithium therapy?

A
  • Information booklet
  • Alert card
  • Record book

These materials help patients understand their treatment and the importance of monitoring.

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63
Q

True or False: Lithium has a long plasma half-life.

A

True

This characteristic affects dosing intervals and monitoring requirements.

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64
Q

Fill in the blank: Lithium levels should be taken _______ hours post-dose.

A

12

Timing of blood draws is critical for accurate measurement of lithium levels.

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65
Q

What ECG changes may occur with lithium use?

A

T wave flattening/inversion

These changes can indicate cardiac effects of lithium therapy.

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66
Q

What blood tests are required for monitoring patients on Statins?

A

LFTs at baseline, 3 months, and 12 months

LFTs refer to Liver Function Tests.

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67
Q

What blood tests must be done prior to treatment with ACE inhibitors?

A

U&E prior to treatment

U&E refers to Urea and Electrolytes.

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68
Q

How often should U&E be monitored for patients on ACE inhibitors after increasing the dose?

A

U&E after increasing dose and at least annually

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69
Q

What tests are required prior to treatment with Amiodarone?

A

TFT, LFT, U&E, CXR prior to treatment

CXR refers to Chest X-Ray.

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70
Q

How frequently should TFT and LFT be monitored for patients on Amiodarone?

A

Every 6 months

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71
Q

What tests are required for monitoring patients on Methotrexate?

A

FBC, LFT, U&E

FBC refers to Full Blood Count.

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72
Q

What is the monitoring recommendation for FBC and renal and LFTs before starting Methotrexate?

A

FBC and renal and LFTs before starting treatment and repeated weekly until therapy stabilised, thereafter every 2-3 months

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73
Q

What tests should be done before treatment with Azathioprine?

A

FBC, LFT before treatment

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74
Q

How often should FBC be monitored for the first 4 weeks of Azathioprine treatment?

A

Weekly for the first 4 weeks

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75
Q

What is the monitoring schedule for FBC and LFT for patients on Azathioprine after the first 4 weeks?

A

Every 3 months

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76
Q

What tests are required prior to treatment with Lithium?

A

Lithium level, TFT, U&E

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77
Q

How often should Lithium levels be monitored until stabilized?

A

Weekly until stabilised

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78
Q

What is the monitoring schedule for TFT and U&E for patients on Lithium?

A

Every 6 months

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79
Q

What tests should be done before treatment with Sodium Valproate?

A

LFT, FBC before treatment

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80
Q

How often should LFT be monitored during the first 6 months of Sodium Valproate treatment?

A

Periodically

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81
Q

What tests are required before treatment with Glitazones?

A

LFT before treatment

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82
Q

How often should LFT be monitored during treatment with Glitazones?

A

Regularly

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83
Q

What is a common feature of Patau syndrome (trisomy 13)?

A

Microcephalic, small eyes

Other features include cleft lip/palate, polydactyly, and scalp lesions.

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84
Q

What are typical characteristics of Edward’s syndrome (trisomy 18)?

A

Micrognathia, low-set ears, rocker bottom feet, overlapping of fingers

These features are often used for diagnosis.

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85
Q

What are the main symptoms of Fragile X syndrome?

A

Learning difficulties, macrocephaly, long face, large ears, macro-orchidism

Fragile X is the most common inherited cause of intellectual disability.

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86
Q

Which features are associated with Noonan syndrome?

A

Webbed neck, pectus excavatum, short stature, pulmonary stenosis

Noonan syndrome can present with various congenital heart defects.

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87
Q

What are the defining characteristics of Pierre-Robin syndrome?

A

Micrognathia, posterior displacement of the tongue, cleft palate

The posterior tongue displacement may result in upper airway obstruction.

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88
Q

List the features of Prader-Willi syndrome.

A

Hypotonia, hypogonadism, obesity

This syndrome is known for its insatiable appetite leading to obesity.

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89
Q

What features are commonly seen in William’s syndrome?

A

Short stature, learning difficulties, friendly extrovert personality, transient neonatal hypercalcaemia, supravalvular aortic stenosis

Individuals often have a distinctive facial appearance.

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90
Q

What is a characteristic cry associated with Cri du chat syndrome?

A

Characteristic cry due to larynx and neurological problems

Other features include feeding difficulties, learning difficulties, and microcephaly.

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91
Q

True or False: Treacher-Collins syndrome is autosomal recessive.

A

False

Treacher-Collins syndrome is autosomal dominant, often with a family history.

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92
Q

Fill in the blank: Cri du chat syndrome is caused by a _______ on chromosome 5p.

A

deletion

This deletion leads to the various features associated with the syndrome.

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93
Q

What is Turner’s syndrome?

A

A chromosomal disorder affecting around 1 in 2,500 females caused by the presence of only one sex chromosome (X) or a deletion of the short arm of one of the X chromosomes.

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94
Q

What is the chromosomal notation for Turner’s syndrome?

A

45,XO or 45,X

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95
Q

List three physical features commonly associated with Turner’s syndrome.

A
  • Short stature
  • Shield chest, widely spaced nipples
  • Webbed neck
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96
Q

What are two serious long-term health problems for women with Turner’s syndrome?

A
  • Aortic dilatation
  • Aortic dissection
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97
Q

Why is regular monitoring important in adult life for women with Turner’s syndrome?

A

To check for complications related to aortic dilatation and dissection.

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98
Q

What is primary amenorrhoea?

A

The absence of menstrual periods in women with Turner’s syndrome.

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99
Q

What is cystic hygroma, and when is it often diagnosed?

A

A fluid-filled sac often diagnosed prenatally.

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100
Q

What is a common dental feature in individuals with Turner’s syndrome?

A

High-arched palate

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101
Q

What skeletal abnormality is often seen in Turner’s syndrome?

A

Short fourth metacarpal

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102
Q

What is the most common renal abnormality in Turner’s syndrome?

A

Horseshoe kidney

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103
Q

What are gonadotrophin levels like in individuals with Turner’s syndrome?

A

Elevated

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104
Q

What endocrine disorder is much more common in Turner’s syndrome?

A

Hypothyroidism

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105
Q

True or False: There is an increased incidence of autoimmune disease in Turner’s syndrome.

A

True

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106
Q

Name an autoimmune disease that has a higher incidence in Turner’s syndrome.

A

Autoimmune thyroiditis

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107
Q

What gastrointestinal condition is more common in individuals with Turner’s syndrome?

A

Crohn’s disease

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108
Q

What percentage of individuals with Turner’s syndrome have a bicuspid aortic valve?

A

15%

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109
Q

What percentage of individuals with Turner’s syndrome may have coarctation of the aorta?

A

5-10%

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110
Q

What condition can cause lymphoedema in neonates with Turner’s syndrome?

A

Lymphoedema, especially in the feet

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111
Q

Fill in the blank: Turner’s syndrome is a chromosomal disorder affecting around 1 in ______ females.

A

2,500

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112
Q

What is the LH and testosterone level in primary hypogonadism (Klinefelter’s syndrome)?

A

LH: High, Testosterone: Low

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113
Q

What are the LH and testosterone levels in hypogonadotrophic hypogonadism (Kallman’s syndrome)?

A

LH: Low, Testosterone: Low

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114
Q

What are the LH and testosterone levels in androgen insensitivity syndrome?

A

LH: High, Testosterone: Normal/high

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115
Q

What is the LH and testosterone level in testosterone-secreting tumour?

A

LH: Low, Testosterone: High

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116
Q

What is the karyotype associated with Klinefelter’s syndrome?

A

47, XXY

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117
Q

List the features of Klinefelter’s syndrome.

A
  • Often taller than average
  • Lack of secondary sexual characteristics
  • Small, firm testes
  • Infertile
  • Gynaecomastia
  • Elevated gonadotrophin levels
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118
Q

How is Klinefelter’s syndrome diagnosed?

A

By chromosomal analysis

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119
Q

What causes Kallman’s syndrome?

A

Failure of GnRH-secreting neurons to migrate to the hypothalamus

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120
Q

What key symptom is associated with Kallman’s syndrome?

A

Lack of smell (anosmia)

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121
Q

List the features of Kallman’s syndrome.

A
  • Delayed puberty
  • Hypogonadism
  • Cryptorchidism
  • Anosmia
  • Low sex hormone levels
  • Inappropriately low/normal LH, FSH levels
  • Typically normal or above average height
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122
Q

What additional defects may be seen in some patients with Kallman’s syndrome?

A
  • Cleft lip/palate
  • Visual/hearing defects
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123
Q

What is the genetic basis of androgen insensitivity syndrome?

A

X-linked recessive condition

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124
Q

What is the phenotype of genotypically male children with androgen insensitivity syndrome?

A

Female phenotype

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125
Q

What is the new term for testicular feminisation syndrome?

A

Complete androgen insensitivity syndrome

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126
Q

List the features of androgen insensitivity syndrome.

A
  • Primary amenorrhea
  • Undescended testes
  • Groin swellings
  • Breast development due to conversion of testosterone to oestradiol
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127
Q

How is androgen insensitivity syndrome diagnosed?

A

Buccal smear or chromosomal analysis to reveal 46XY genotype

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128
Q

What is the management approach for androgen insensitivity syndrome?

A
  • Counselling to raise child as female
  • Bilateral orchidectomy
  • Oestrogen therapy
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129
Q

What is the most common malignancy in men aged 20-30 years?

A

Testicular cancer

Testicular cancer primarily affects younger men, highlighting the importance of awareness and early detection.

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130
Q

What percentage of testicular cancer cases are germ-cell tumours?

A

Around 95%

Germ-cell tumours are the predominant form of testicular cancer.

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131
Q

What are the two main categories of germ cell tumours?

A

Seminomas and non-seminomas

Non-seminomas include embryonal, yolk sac, teratoma, and choriocarcinoma.

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132
Q

Name two types of non-germ cell tumours.

A
  • Leydig cell tumours
  • Sarcomas

Non-germ cell tumours represent a different classification than germ cell tumours.

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133
Q

At what age is the peak incidence for teratomas?

A

25 years

Understanding peak incidence helps in identifying at-risk populations.

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134
Q

At what age is the peak incidence for seminomas?

A

35 years

This age distribution is crucial for screening and awareness.

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135
Q

What are some risk factors for testicular cancer?

A
  • Infertility (increases risk by a factor of 3)
  • Cryptorchidism
  • Family history
  • Klinefelter’s syndrome
  • Mumps orchitis

Knowledge of these risk factors can aid in early detection and management.

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136
Q

What is the most common presenting symptom of testicular cancer?

A

A painless lump

Early recognition of symptoms can lead to timely diagnosis.

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137
Q

What additional symptoms may occur in a minority of men with testicular cancer?

A
  • Pain
  • Hydrocele
  • Gynaecomastia

These symptoms can vary and may indicate underlying pathology.

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138
Q

What hormonal changes contribute to gynaecomastia in testicular cancer?

A

Increased oestrogen:androgen ratio

This hormonal imbalance is significant in the pathophysiology of testicular cancer.

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139
Q

What is the elevation of hCG in seminomas?

A

May be elevated in around 20%

This is important for diagnosis and monitoring treatment response.

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140
Q

What tumour markers are elevated in non-seminomas?

A

AFP and/or beta-hCG in 80-85%

These markers are critical for identifying and managing non-seminomatous germ cell tumours.

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141
Q

What is the first-line diagnostic tool for testicular cancer?

A

Ultrasound

Ultrasound is a non-invasive method essential for initial evaluation.

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142
Q

What are the primary management options for testicular cancer?

A
  • Orchidectomy
  • Chemotherapy
  • Radiotherapy

Management strategies depend on the type and stage of the tumour.

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143
Q

What is the 5-year survival rate for seminomas at Stage I?

A

Around 95%

This high survival rate underscores the effectiveness of early treatment.

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144
Q

What is the 5-year survival rate for teratomas at Stage I?

A

Around 85%

The prognosis remains favorable with early intervention.

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145
Q

What type of conditions are often thought to be ‘metabolic’?

A

Autosomal recessive conditions

This contrasts with autosomal dominant conditions which are often considered ‘structural’.

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146
Q

Provide an example of an X-linked recessive metabolic condition.

A

Hunter’s syndrome

Another example is G6PD deficiency.

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147
Q

Which conditions are notable exceptions to the classification of metabolic and structural?

A

Some ‘metabolic’ conditions such as Hunter’s and G6PD are X-linked recessive, while some ‘structural’ conditions such as ataxia telangiectasia and Friedreich’s ataxia are autosomal recessive.

This highlights the complexity in classifying genetic conditions.

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148
Q

List three autosomal recessive conditions.

A
  • Albinism
  • Ataxic telangiectasia
  • Congenital adrenal hyperplasia
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149
Q

Which autosomal recessive condition is characterized by thick, sticky mucus production?

A

Cystic fibrosis

This condition affects the lungs and digestive system.

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150
Q

What is Friedreich’s ataxia classified as?

A

Autosomal recessive

It is a genetic condition that affects the nervous system and the heart.

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151
Q

Fill in the blank: Gilbert’s syndrome is still a matter of debate and many textbooks will list it as _______ dominant.

A

autosomal

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152
Q

Name a condition associated with lipid storage disorders that is autosomal recessive.

A

Tay-Sach’s

Other examples include Gaucher and Niemann-Pick diseases.

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153
Q

Which autosomal recessive condition is characterized by the body’s inability to process phenylalanine?

A

PKU

PKU stands for phenylketonuria.

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154
Q

True or False: Sickle cell anemia is an autosomal recessive condition.

A

True

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155
Q

What is the classification of Wilson’s disease?

A

Autosomal recessive

This condition leads to excessive copper accumulation in the body.

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156
Q

List two conditions that can cause periodic paralysis and are classified as autosomal dominant.

A
  • Hyperlipidemia type II
  • Hypokalemic periodic paralysis
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157
Q

What is the genetic classification of Familial Mediterranean Fever?

A

Autosomal recessive

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158
Q

What type of inheritance pattern does Haemochromatosis follow?

A

Autosomal recessive

This condition leads to excessive iron absorption in the body.

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159
Q

Fill in the blank: The condition known as Cystinuria is classified as _______ recessive.

A

autosomal

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160
Q

What is the classification of Glycogen storage disease?

A

Autosomal recessive

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161
Q

What type of inheritance do conditions like Achondroplasia have?

A

Autosomal dominant

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162
Q

Name a condition that is classified as autosomal dominant.

A

Achondroplasia

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163
Q

Name a condition associated with autosomal dominant inheritance that affects the skin and connective tissue.

A

Ehlers-Danlos syndrome

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164
Q

Which autosomal dominant condition is characterized by the presence of multiple colon polyps?

A

Familial adenomatous polyposis

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165
Q

What is the inheritance pattern of Huntington’s disease?

A

Autosomal dominant

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166
Q

True or False: Neurofibromatosis is an autosomal dominant condition.

A

True

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167
Q

Fill in the blank: _______ syndrome is an autosomal dominant condition that affects connective tissues.

A

Marfan’s

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168
Q

What is the inheritance pattern of Von Willebrand’s disease type 3?

A

Autosomal recessive

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169
Q

List three conditions that are autosomal dominant.

A
  • Acute intermittent porphyria
  • Myotonic dystrophy
  • Retinoblastoma
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170
Q

Which autosomal dominant condition is associated with a deficiency of Antithrombin III?

A

Antithrombin III deficiency

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171
Q

What is the relationship between hereditary haemorrhagic telangiectasia and inheritance?

A

It is autosomal dominant

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172
Q

Fill in the blank: _______ syndrome is associated with an increased risk of developing colorectal cancer and is inherited in an autosomal dominant manner.

A

Hereditary non-polyposis colorectal carcinoma

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173
Q

Name an autosomal dominant condition that can lead to malignant hyperthermia.

A

Malignant hyperthermia

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174
Q

True or False: Osteogenesis imperfecta is an autosomal dominant condition.

A

True

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175
Q

What type of inheritance does Peutz-Jeghers syndrome follow?

A

Autosomal dominant

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176
Q

List two conditions that are classified as autosomal dominant.

A
  • Hyperlipidaemia type II
  • Noonan syndrome
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177
Q

Which autosomal dominant condition is characterized by the formation of tumors in the nervous system?

A

Neurofibromatosis

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178
Q

Fill in the blank: _______ syndrome is a genetic disorder characterized by the development of tumors and is inherited in an autosomal dominant pattern.

A

Tuberous sclerosis

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179
Q

What is a common feature of many autosomal dominant conditions?

A

They often manifest in individuals with only one copy of the mutated gene.

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180
Q

What conditions do not require school exclusion?

A

Conjunctivitis, Fifth disease (slapped cheek), Roseola, Infectious mononucleosis, Head lice, Threadworms, Hand, foot and mouth

These conditions are generally not contagious enough to warrant exclusion from school.

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181
Q

How long after commencing antibiotics for scarlet fever should a child be excluded from school?

A

24 hours

This is to ensure that the child is no longer contagious.

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182
Q

What is the exclusion period for whooping cough?

A

2 days after commencing antibiotics or 21 days from onset of symptoms if no antibiotics

This ensures that the risk of transmission is minimized.

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183
Q

How many days after the onset of rash should a child with measles be excluded?

A

4 days from onset of rash

This is to prevent the spread of the virus in schools.

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184
Q

What is the exclusion period for rubella?

A

5 days from onset of rash

This helps limit the risk of infection to others.

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185
Q

When can a child return to school after chickenpox?

A

All lesions crusted over or 5 days after the onset of rash

It’s important to ensure that the child is no longer infectious.

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186
Q

What is the exclusion period for mumps?

A

5 days from onset of swollen glands

This time frame is necessary to reduce the risk of spreading the virus.

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187
Q

How long should a child be excluded if they have diarrhea and vomiting?

A

Until symptoms have settled for 48 hours

This is to prevent the spread of infectious agents.

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188
Q

What is the exclusion requirement for impetigo?

A

Until lesions are crusted and healed, or 48 hours after commencing antibiotic treatment

This ensures the child is no longer contagious.

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189
Q

What should be done for a child with scabies regarding school exclusion?

A

Until treated

This is crucial to prevent further spread of scabies.

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190
Q

When can a child return to school after influenza?

A

Until recovered

This helps ensure that the child is fit to participate in school activities.

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191
Q

True or False: Chickenpox is infectious from 2 days before the rash appears to 5 days after the onset of rash.

A

True

This highlights the contagious nature of chickenpox.

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192
Q

What vaccine is given at birth if risk factors are present?

A

BCG vaccine

Given if there are risk factors for tuberculosis, such as a family history in the past 6 months.

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193
Q

What does the ‘6-1 vaccine’ include?

A
  • Diphtheria
  • Tetanus
  • Whooping cough
  • Polio
  • Hib
  • Hepatitis B

Administered at 2, 3, and 4 months.

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194
Q

At what age is the oral rotavirus vaccine administered?

A

2 months and 3 months

It is part of the vaccination schedule for infants.

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195
Q

What vaccine is given at 3 months alongside the ‘6-1 vaccine’?

A

PCV

Pneumococcal conjugate vaccine.

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196
Q

What vaccines are administered at 12-13 months?

A
  • Hib/Men C
  • MMR
  • PCV
  • Men B

These vaccines are crucial for early childhood health.

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197
Q

What is the annual vaccine given between 2-8 years?

A

Flu vaccine

Administered annually to protect against influenza.

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198
Q

What does the ‘4-in-1 pre-school booster’ include?

A
  • Diphtheria
  • Tetanus
  • Whooping cough
  • Polio

Given at 3-4 years of age.

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199
Q

At what age is the HPV vaccination administered?

A

12-13 years

Human papillomavirus vaccination.

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200
Q

What does the ‘3-in-1 teenage booster’ include?

A
  • Tetanus
  • Diphtheria
  • Polio

Given between 13-18 years.

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201
Q

What vaccine has replaced meningitis C for 13-18 year-olds?

A

Meningitis ACWY vaccine

Due to an increased incidence of meningitis W disease.

202
Q

Who is advised to get the Men ACWY vaccine?

A
  • 17-and 18-year-olds in school year 13
  • Students going to university or college for the first time up to the age of 25

Students should contact their GP to receive the vaccine ideally before the academic year starts.

203
Q

What should be done for children with severe or life-threatening asthma?

A

Transfer immediately to hospital

204
Q

What is the SpO2 level indicative of a moderate asthma attack in children aged 2 to 5 years?

A

SpO2 > 92%

205
Q

List the clinical features of a severe asthma attack in children aged 2 to 5 years.

A
  • SpO2 < 92%
  • Too breathless to talk or feed
  • Heart rate > 140/min
  • Respiratory rate > 40/min
  • Use of accessory neck muscles
206
Q

What defines a life-threatening asthma attack in children aged 2 to 5 years?

A
  • SpO2 < 92%
  • Silent chest
  • Poor respiratory effort
  • Agitation
  • Altered consciousness
  • Cyanosis
207
Q

What should be attempted to measure in children greater than 5 years of age during an asthma attack?

A

PEF (Peak Expiratory Flow)

208
Q

What is the SpO2 level indicative of a moderate asthma attack in children greater than 5 years?

A

SpO2 > 92%

209
Q

What are the clinical features of a severe asthma attack in children greater than 5 years?

A
  • SpO2 < 92%
  • PEF 33-50% best or predicted
  • Can’t complete sentences in one breath or too breathless to talk or feed
  • Heart rate > 125/min
  • Respiratory rate > 30/min
  • Use of accessory neck muscles
210
Q

What defines a life-threatening asthma attack in children greater than 5 years?

A
  • SpO2 < 92%
  • PEF < 33% best or predicted
  • Silent chest
  • Poor respiratory effort
  • Altered consciousness
  • Cyanosis
211
Q

What is the first line of treatment for children with mild to moderate acute asthma?

A

Bronchodilator therapy

212
Q

How should a beta-2 agonist be administered to children with mild to moderate acute asthma?

A

Via a spacer (close-fitting mask for children < 3 years), 1 puff every 30-60 seconds up to a maximum of 10 puffs

213
Q

What should be done if symptoms are not controlled after administering a beta-2 agonist?

A

Repeat beta-2 agonist and refer to hospital

214
Q

What type of therapy should be given to all children with an asthma exacerbation?

A

Steroid therapy

215
Q

What is the duration of steroid treatment for children with asthma exacerbation?

216
Q

What is the usual prednisolone dose for children aged 2-5 years?

A

20 mg od/1-2 mg/kg od (max 40mg)

217
Q

What is the usual prednisolone dose for children greater than 5 years?

A

30 - 40 mg od/1-2 mg/kg od (max 40mg)

218
Q

What method should be used to measure temperature in children less than 4 weeks old?

A

An electronic thermometer in the axilla

This method is recommended for accurate temperature measurement in very young infants.

219
Q

What types of thermometers can be used for measuring temperature in children older than 4 weeks?

A

Electronic/chemical dot thermometer in the axilla or an infra-red tympanic thermometer

These thermometers provide alternative methods for temperature measurement in older children.

220
Q

What does the green traffic light indicate for fever in children?

A

Low risk

Normal colour, responds normally to social cues, normal circulation and hydration

221
Q

What are the signs of the green category?

A

• Normal colour
• Responds normally to social cues
• Strong normal cry/not crying
• Normal skin and eyes
• Moist mucous membranes
• No amber or red signs

These indicate a low risk for serious illness.

222
Q

What does the amber traffic light indicate for fever in children?

A

Intermediate risk

Signs include pallor and decreased responsiveness.

223
Q

What are the signs of the amber category?

A

• Pallor reported by parent/carer
• Not responding normally to social cues
• No smile
• Wakes only with prolonged stimulation
• Decreased activity
• Tachypnoea
• Tachycardia
• Capillary refill time >=3 seconds
• Dry mucous membranes
• Poor feeding in infants
• Reduced urine output

Specific age and temperature criteria also apply.

224
Q

What respiratory signs indicate a child is in the amber category?

A

• Nasal flaring
• Respiratory rate >50 breaths/minute (age 6-12 months)
• Respiratory rate >40 breaths/minute (age >12 months)

These signs suggest a moderate risk of serious illness.

225
Q

What is the tachycardia threshold for children under 12 months in the amber category?

A

> 160 beats/minute

Tachycardia thresholds vary by age.

226
Q

What does the red traffic light indicate for fever in children?

A

High risk

Immediate medical attention is required.

227
Q

What are the signs of the red category?

A

• Pale/mottled/ashen/blue colour
• No response to social cues
• Appears ill to a healthcare professional
• Does not wake or if roused does not stay awake
• Weak, high-pitched or continuous cry
• Grunting
• Respiratory rate >60 breaths/minute
• Oxygen saturation <=95% in air
• Non-blanching rash
• Bulging fontanelle
• Neck stiffness
• Status epilepticus
• Focal neurological signs
• Focal seizures

These signs indicate a severe and potentially life-threatening condition.

228
Q

What should be done if a child is categorized as amber?

A

Provide parents with a safety net or refer to a paediatric specialist

Safety net includes information on warning symptoms and how to access further healthcare.

229
Q

What should be done if a child is categorized as red?

A

Refer child urgently to a paediatric specialist

Immediate action is critical for high-risk indicators.

230
Q

True or False: Oral antibiotics should be prescribed to children with fever without apparent source.

A

False

Antibiotics should not be prescribed without a clear source of infection.

231
Q

If pneumonia is suspected but the child is not referred to hospital, what is the protocol regarding chest x-rays?

A

A chest x-ray does not need to be routinely performed

This applies only if the child is not being referred.

232
Q

What is the prevalence of headache in boys and girls before puberty?

A

Equally as common in boys and girls until puberty, then a strong (3:1) female preponderance.

233
Q

What is the most common cause of primary headache in children?

A

Migraine without aura.

234
Q

What are the criteria for pediatric migraine without aura according to the International Headache Society?

A

A. >= 5 attacks fulfilling features B to D
B. Headache lasting 4-72 hours
C. At least two of the following:
* bilateral or unilateral location
* pulsating quality
* moderate to severe intensity
* aggravated by routine physical activity
D. At least one of the following:
* nausea and/or vomiting
* photophobia and phonophobia

235
Q

What is the preferred acute management medication for pediatric migraine?

A

Ibuprofen is thought to be more effective than paracetamol.

236
Q

At what age can triptans be used for children, and what is the only licensed triptan with proven efficacy?

A

Triptans may be used in children >= 12 years; sumatriptan nasal spray is licensed.

237
Q

What are some side effects of triptans?

A
  • Tingling
  • Heat
  • Heaviness/pressure sensations
238
Q

What is the status of oral triptans for individuals under 18 years?

A

Oral triptans are not currently licensed in people < 18 years.

239
Q

What are the first-line preventative treatments for pediatric migraine according to the GOSH website?

A
  • Pizotifen
  • Propranolol
240
Q

What are the second-line preventative treatments for pediatric migraine?

A
  • Valproate
  • Topiramate
  • Amitryptiline
241
Q

What is the second most common cause of headache in children?

A

Tension-type headache (TTH).

242
Q

What are the diagnostic criteria for tension-type headache in children?

A

A. At least 10 previous headache episodes fulfilling features B to D
B. Headache lasting from 30 minutes to 7 days
C. At least two of the following:
* pressing/tightening quality
* mild or moderate intensity
* bilateral location
* no aggravation by routine physical activity
D. Both of the following:
* no nausea or vomiting
* photophobia and phonophobia, or one, but not the other is present

243
Q

What is the function of the trabecular network?

A

It offers increased resistance to aqueous outflow, causing increased IOP.

244
Q

What is the aim of treatment for increased intra-ocular pressure (IOP)?

A

To lower intra-ocular pressure to prevent progressive loss of visual field.

245
Q

What does NICE guidelines recommend as first-line treatment for IOP of ≥ 24 mmHg?

A

360° selective laser trabeculoplasty (SLT).

246
Q

What are the benefits of 360° SLT?

A

It can delay the need for eye drops and reduce but not eliminate the chance they will be needed.

247
Q

What may be needed at a later date after the first 360° SLT procedure?

A

A second 360° SLT procedure.

248
Q

What are the second-line treatments according to NICE?

A

Prostaglandin analogue (PGA) eyedrops.

249
Q

List the next line of treatments for increased IOP.

A
  • Beta-blocker eye drops
  • Carbonic anhydrase inhibitor eye drops
  • Sympathomimetic eye drops
  • Surgery (trabeculectomy) in refractory cases.
250
Q

What is the action of prostaglandin analogues (e.g. latanoprost)?

A

Increases uveoscleral outflow with once daily administration.

251
Q

What are the adverse effects of prostaglandin analogues?

A
  • Brown pigmentation of the iris
  • Increased eyelash length.
252
Q

What is the effect of beta-blockers (e.g. timolol, betaxolol) on aqueous production?

A

Reduces aqueous production.

253
Q

Who should avoid beta-blockers?

A

Asthmatics and patients with heart block.

254
Q

What is the action of sympathomimetics (e.g. brimonidine)?

A

Reduces aqueous production and increases outflow.

255
Q

What should be avoided when taking sympathomimetics?

A

MAOI or tricyclic antidepressants.

256
Q

What are the adverse effects of sympathomimetics?

A

Hyperaemia.

257
Q

What is the action of carbonic anhydrase inhibitors (e.g. Dorzolamide)?

A

Reduces aqueous production.

258
Q

What adverse reactions may occur due to systemic absorption of carbonic anhydrase inhibitors?

A

Sulphonamide-like reactions.

259
Q

What is the action of miotics (e.g. pilocarpine)?

A

Increases uveoscleral outflow.

260
Q

What is a direct parasympathomimetic used to treat Acute glaucoma?

A

Pilocarpine

Pilocarpine causes contraction of the ciliary muscle, leading to the opening of the trabecular meshwork and increased outflow of aqueous humour.

261
Q

What is the mechanism of action of beta-blockers in treating Acute glaucoma?

A

Decreases aqueous humour production

An example of a beta-blocker used is timolol.

262
Q

What is an alpha-2 agonist used in the treatment of Acute glaucoma?

A

Apraclonidine

Apraclonidine has a dual mechanism of decreasing aqueous humour production and increasing uveoscleral outflow.

263
Q

What is the role of intravenous acetazolamide in treating Acute glaucoma?

A

Reduces aqueous secretions

It is used to lower intraocular pressure in acute situations.

264
Q

What is recommended alongside other treatments to reduce inflammation in Acute glaucoma?

A

Topical steroids

Some guidelines suggest using topical steroids as part of the management plan.

265
Q

What is the definitive management procedure for Acute glaucoma?

A

Laser peripheral iridotomy

This procedure creates a tiny hole in the peripheral iris to allow aqueous humour to flow to the angle.

266
Q

Fill in the blank: A direct parasympathomimetic like _______ causes contraction of the ciliary muscle.

A

pilocarpine

267
Q

True or False: Timolol is an alpha-2 agonist used in the treatment of Acute glaucoma.

A

False

Timolol is a beta-blocker, while apraclonidine is the alpha-2 agonist.

268
Q

What is the driving rule for hypertension?

A

Can drive unless treatment causes unacceptable side effects; no need to notify DVLA.

If Group 2 Entitlement, disqualified from driving if resting BP consistently 180 mmHg systolic or more and/or 100 mmHg diastolic or more.

269
Q

What is the required off-driving period after elective angioplasty?

A

1 week off driving.

270
Q

How long must a patient refrain from driving after CABG?

A

4 weeks off driving.

271
Q

What is the driving restriction duration for acute coronary syndrome?

A

4 weeks off driving; 1 week if successfully treated by angioplasty.

272
Q

When must driving cease for a patient with angina?

A

If symptoms occur at rest or at the wheel.

273
Q

What is the off-driving period after pacemaker insertion?

A

1 week off driving.

274
Q

What are the driving rules for an implantable cardioverter-defibrillator (ICD)?

A

Cease driving for 6 months if implanted for sustained ventricular arrhythmia; 1 month if implanted prophylactically. Permanent bar for Group 2 drivers.

275
Q

How long must a patient refrain from driving after successful catheter ablation for an arrhythmia?

A

2 days off driving.

276
Q

What should patients with an aortic aneurysm of 6 cm or more do?

A

Notify DVLA; licensing permitted subject to annual review.

277
Q

What is the driving restriction for an aortic diameter of 6.5 cm or more?

A

Disqualifies patients from driving.

278
Q

What is the driving rule after a heart transplant?

A

Do not drive for 6 weeks; no need to notify DVLA.

279
Q

What should all patients with epilepsy/seizures do regarding driving?

A

Must not drive and must inform the DVLA

This includes all types of seizures.

280
Q

What is the driving restriction period after a first unprovoked/isolated seizure without relevant abnormalities?

A

6 months off driving

If there are structural abnormalities or epileptiform activity, the period increases to 12 months.

281
Q

What is the driving qualification condition for patients with established epilepsy?

A

Must be free from any seizure for 12 months

A ‘til 70 licence can be restored if there have been no seizures for 5 years.

282
Q

What should patients do while withdrawing from epilepsy medication?

A

Should not drive during withdrawal and for 6 months after last dose

This ensures safety during a sensitive period.

283
Q

What is the driving restriction for a simple faint?

A

No restriction

Simple fainting does not typically affect driving ability.

284
Q

What is the driving restriction for a single episode of syncope that is unexplained?

A

6 months off driving

This is to ensure safety while the cause is investigated.

285
Q

What is the driving restriction for two or more episodes of syncope?

A

12 months off driving

Multiple episodes indicate a higher risk of recurrence.

286
Q

What is the driving restriction after a stroke or TIA if there is no residual neurological deficit?

A

1 month off driving

May not need to inform the DVLA in this case.

287
Q

What is the driving restriction after multiple TIAs over a short period?

A

3 months off driving and inform DVLA

This is due to increased risk of driving impairment.

288
Q

What is the driving restriction after a craniotomy for a meningioma?

A

1 year off driving

If the tumour is benign and no seizure history, reconsideration may be possible after 6 months.

289
Q

What is the driving restriction after a pituitary tumour craniotomy?

A

6 months off driving

Patients can drive when there is no residual impairment affecting safe driving.

290
Q

What should patients with narcolepsy/cataplexy do regarding driving?

A

Cease driving on diagnosis and can restart once symptoms are under satisfactory control

This is essential for safety on the road.

291
Q

What should be done by patients with chronic neurological disorders like multiple sclerosis?

A

Inform the DVLA and complete the PK1 form

This is necessary to assess their fitness to drive.

292
Q

What condition was previously restricted from holding a HGV licence until October 2011?

A

diabetes mellitus

The DVLA changed the rules regarding HGV licences for individuals with diabetes.

293
Q

What are the standards that must be met for a driver with diabetes on insulin to hold a HGV licence?

A

Standards include:
* No severe hypoglycaemic event in the previous 12 months
* Full hypoglycaemic awareness
* Adequate control of the condition through regular blood glucose monitoring
* Understanding of hypoglycaemia risks
* No other debarring complications of diabetes

These standards also apply to patients using other hypoglycaemic inducing drugs.

294
Q

What form must insulin-using patients complete to apply for a Group 2 (HGV) licence?

A

VDIAB1I form

This form is specifically for patients on insulin who want to apply for a HGV licence.

295
Q

What conditions allow a patient on insulin to drive a car?

A

Conditions include:
* Hypoglycaemic awareness
* No more than one episode of hypoglycaemia requiring assistance in the last 12 months
* No relevant visual impairment

Drivers are usually contacted by the DVLA.

296
Q

Do drivers taking tablets or exenatide need to notify the DVLA?

A

No, unless the tablets may induce hypoglycaemia

In such cases, they must not have experienced more than one episode requiring assistance in the last 12 months.

297
Q

What is the requirement for drivers whose diabetes is controlled by diet alone?

A

No requirement to inform DVLA

This applies to individuals managing their diabetes strictly through dietary measures.

298
Q

How often must blood glucose monitoring be conducted to demonstrate adequate control for HGV licence applicants?

A

At least twice daily

This includes monitoring at times relevant to driving.

299
Q

What additional feature should blood glucose meters have for applicants to demonstrate adequate control?

A

Memory function

Applicants should have used these meters for at least 3 months prior to application.

300
Q

What are the rules for individuals with severe anxiety or depression regarding driving?

A

Must not drive and must notify the DVLA

Applies if there are significant memory problems, concentration problems, agitation, behavioral disturbance, or suicidal thoughts.

301
Q

What is required for individuals experiencing acute psychotic disorder?

A

Must not drive during acute illness and must notify the DVLA

This applies during the period of acute illness.

302
Q

What are the driving regulations for individuals with hypomania or mania?

A

Must not drive during acute illness and must notify the DVLA

This rule is in place during the acute phase of the condition.

303
Q

What should individuals with schizophrenia do regarding driving?

A

Must not drive during acute illness and must notify the DVLA

This is required during the acute phase of the illness.

304
Q

Can individuals with pervasive developmental disorders and ADHD drive?

A

May be able to drive but must inform the DVLA

Notification to the DVLA is necessary in this case.

305
Q

What is the driving status for individuals with mild cognitive impairment?

A

May drive and need not inform the DVLA

This condition does not require notification.

306
Q

What must individuals with dementia do regarding driving?

A

May be able to drive but must inform the DVLA

It is important to notify the DVLA.

307
Q

What are the driving regulations for individuals with mild learning disability?

A

May be able to drive but must inform the DVLA

Notification to the DVLA is required.

308
Q

What is the driving status for individuals with severe disability?

A

Must not drive and must notify the DVLA

This applies to those with significant impairments.

309
Q

Can individuals with personality disorders drive?

A

May be able to drive but must inform the DVLA

It is necessary to notify the DVLA about their condition.

310
Q

What is the minimum period required for licence revocation or refusal due to persistent alcohol misuse?

A

6 months of controlled drinking or abstinence with normalisation of blood parameters

Persistent alcohol misuse is confirmed by medical enquiry and/or abnormal blood markers.

311
Q

How long is the licence revocation period for alcohol dependency?

A

1 year

This is in line with the guidelines for persistent alcohol misuse.

312
Q

What substances lead to a minimum 6 month licence refusal or revocation if there is persistent use or dependency?

A
  • Cannabis
  • Amphetamines
  • Ecstasy
  • LSD

Medical enquiry confirmation is required for these substances.

313
Q

What is the minimum period for licence refusal or revocation for heroin, cocaine, or methadone dependency?

A

1 year

A consultant report may be required upon reapplication.

314
Q

True or False: The rules for drivers of heavy goods vehicles are the same as for car and motorcycle drivers regarding drug and alcohol misuse.

A

False

The rules for heavy goods vehicles tend to be much stricter.

315
Q

Fill in the blank: Persistent alcohol misuse is defined by the DVLA as ‘a state which, because of consumption of alcohol, causes disturbance of behavior, related disease or other consequences, likely to cause the patient, his/her family or society harm now, or in the future, and which may or may not be associated with _______.

A

dependency

This definition highlights the potential harm caused by alcohol misuse.

316
Q

What must drivers with visual field defects do?

A

Driving must cease unless confirmed able to meet recommended national guidelines for visual field

This ensures safety on the road due to potential limitations in vision.

317
Q

What is required of drivers with monocular vision?

A

Must notify DVLA

They may drive if acuity and visual field is normal in the remaining eye.

318
Q

What should a driver with blepharospasm seek?

A

Consultant opinion is required

This is necessary to assess their ability to drive safely.

319
Q

Which drivers have stricter rules according to the DVLA guidelines?

A

Drivers of heavy goods vehicles

These drivers are subject to more stringent regulations due to the nature of their vehicles.

320
Q

What are the three classifications of diabetic retinopathy?

A

Non-proliferative diabetic retinopathy (NPDR), proliferative retinopathy (PDR), maculopathy

These classifications help in assessing the severity and treatment options for diabetic retinopathy.

321
Q

What characterizes Mild Non-proliferative diabetic retinopathy (NPDR)?

A

1 or more microaneurysm

Mild NPDR indicates the earliest stage of diabetic retinopathy.

322
Q

List the features of Moderate Non-proliferative diabetic retinopathy (NPDR).

A
  • microaneurysms
  • blot haemorrhages
  • hard exudates
  • cotton wool spots
  • venous beading/looping
  • intraretinal microvascular abnormalities (IRMA) less severe than in severe NPDR

Moderate NPDR shows more significant changes in the retina.

323
Q

What defines Severe Non-proliferative diabetic retinopathy (NPDR)?

A
  • blot haemorrhages and microaneurysms in 4 quadrants
  • venous beading in at least 2 quadrants
  • IRMA in at least 1 quadrant

Severe NPDR indicates a high risk of progression to proliferative diabetic retinopathy.

324
Q

What are the key features of Proliferative diabetic retinopathy (PDR)?

A
  • retinal neovascularisation
  • fibrous tissue forming anterior to retinal disc
  • more common in Type I DM
  • 50% blind in 5 years

PDR is a more advanced stage of diabetic retinopathy with significant risk of vision loss.

325
Q

What is maculopathy based on?

A

Location rather than severity

Maculopathy can be serious regardless of the severity of other changes in the retina.

326
Q

What are the key features of maculopathy?

A
  • hard exudates
  • other ‘background’ changes on macula
  • check visual acuity
  • more common in Type II DM

Maculopathy focuses on the macula, which is crucial for central vision.

327
Q

What is the general management approach for all diabetic retinopathy patients?

A
  • optimise glycaemic control
  • manage blood pressure
  • control hyperlipidemia
  • regular review by ophthalmology

Effective management can slow the progression of diabetic retinopathy.

328
Q

What treatment is indicated for maculopathy if there is a change in visual acuity?

A

Intravitreal vascular endothelial growth factor (VEGF) inhibitors

These inhibitors can help improve visual outcomes in patients with maculopathy.

329
Q

What is recommended for Non-proliferative retinopathy management?

A

Regular observation

Severe or very severe cases may require panretinal laser photocoagulation.

330
Q

What is the treatment for Proliferative retinopathy?

A
  • panretinal laser photocoagulation
  • intravitreal VEGF inhibitors
  • vitreoretinal surgery if severe or vitreous haemorrhage

These treatments aim to prevent vision loss and manage complications.

331
Q

True or False: Following treatment for proliferative retinopathy, around 50% of patients develop a noticeable reduction in their visual fields.

A

True

This reduction is due to the scarring of peripheral retinal tissue.

332
Q

What are some complications of proliferative retinopathy treatments?

A
  • decrease in night vision
  • generalised decrease in visual acuity
  • macular oedema

Night vision is primarily affected due to the role of rod cells in low light conditions.

333
Q

Fill in the blank: Examples of intravitreal VEGF inhibitors include _______.

A

ranibizumab

These medications are often used alongside laser treatments.

334
Q

What is the role of intravitreal VEGF inhibitors in the treatment of proliferative diabetic retinopathy?

A

They slow progression and improve visual acuity

Combining these inhibitors with laser treatment enhances patient outcomes.

335
Q

What is the function of Nerve I (Olfactory)?

A

Smell

Nerve I is responsible for the sense of smell.

336
Q

What is the clinical pathway for Nerve I (Olfactory)?

A

Cribriform plate

This is the structure through which the olfactory nerve fibers pass.

337
Q

What is the function of Nerve II (Optic)?

A

Sight

Nerve II is responsible for vision.

338
Q

What is the clinical pathway for Nerve II (Optic)?

A

Optic canal

This is the passage through which the optic nerve travels.

339
Q

What are the functions of Nerve III (Oculomotor)?

A
  • Eye movement (MR, IO, SR, IR)
  • Pupil constriction
  • Accommodation
  • Eyelid opening

MR: Medial Rectus, IO: Inferior Oblique, SR: Superior Rectus, IR: Inferior Rectus.

340
Q

What are the clinical signs of a palsy in Nerve III (Oculomotor)?

A
  • Ptosis ‘down and out’ eye
  • Dilated, fixed pupil

These symptoms indicate dysfunction of the oculomotor nerve.

341
Q

What is the clinical pathway for Nerve III (Oculomotor)?

A

Superior orbital fissure (SOF)

This is the foramen through which the oculomotor nerve exits the skull.

342
Q

What is the function of Nerve IV (Trochlear)?

A

Eye movement (SO)

Trochlear nerve is primarily responsible for the movement of the superior oblique muscle.

343
Q

What is a clinical sign of a palsy in Nerve IV (Trochlear)?

A

Defective downward gaze → vertical diplopia

Vertical diplopia occurs when the eyes are not properly aligned.

344
Q

What is the clinical pathway for Nerve IV (Trochlear)?

A

Superior orbital fissure (SOF)

This is the foramen through which the trochlear nerve travels.

345
Q

What are the functions of Nerve V (Trigeminal)?

A
  • Facial sensation
  • Mastication

Trigeminal nerve has three branches: V1, V2, and V3.

346
Q

What lesions may occur with Nerve V (Trigeminal)?

A
  • Trigeminal neuralgia
  • Loss of corneal reflex (afferent)
  • Loss of facial sensation
  • Paralysis of mastication muscles
  • Deviation of jaw to weak side

These are common clinical manifestations related to trigeminal nerve lesions.

347
Q

What is the clinical pathway for Nerve V (Trigeminal)?

A

V1: SOF, V2: Foramen rotundum, V3: Foramen ovale

Each branch of the trigeminal nerve exits the skull through different foramina.

348
Q

What is the function of Nerve VI (Abducens)?

A

Eye movement (LR)

Abducens nerve controls the lateral rectus muscle.

349
Q

What is a clinical sign of a palsy in Nerve VI (Abducens)?

A

Defective abduction → horizontal diplopia

Horizontal diplopia occurs when the eyes fail to move laterally properly.

350
Q

What is the clinical pathway for Nerve VI (Abducens)?

A

Superior orbital fissure (SOF)

This is the foramen through which the abducens nerve exits the skull.

351
Q

What are the functions of Nerve VII (Facial)?

A
  • Facial movement
  • Taste (anterior 2/3rds of tongue)
  • Lacrimation
  • Salivation

Facial nerve controls muscles of facial expression and taste sensations.

352
Q

What lesions may occur with Nerve VII (Facial)?

A
  • Flaccid paralysis of upper + lower face
  • Loss of corneal reflex (efferent)
  • Loss of taste
  • Hyperacusis

These signs indicate dysfunction of the facial nerve.

353
Q

What is the clinical pathway for Nerve VII (Facial)?

A

Internal auditory meatus

This is the structure through which the facial nerve exits the skull.

354
Q

What are the functions of Nerve VIII (Vestibulocochlear)?

A
  • Hearing
  • Balance

Vestibulocochlear nerve is responsible for auditory and vestibular functions.

355
Q

What lesions may occur with Nerve VIII (Vestibulocochlear)?

A
  • Hearing loss
  • Vertigo
  • Nystagmus
  • Acoustic neuromas

These conditions are associated with vestibulocochlear nerve dysfunction.

356
Q

What is the clinical pathway for Nerve VIII (Vestibulocochlear)?

A

Internal auditory meatus

This is the foramen through which the vestibulocochlear nerve exits the skull.

357
Q

What are the functions of Nerve IX (Glossopharyngeal)?

A
  • Taste (posterior 1/3rd of tongue)
  • Salivation
  • Swallowing
  • Mediates input from carotid body & sinus

Glossopharyngeal nerve is involved in taste and autonomic functions.

358
Q

What lesions may occur with Nerve IX (Glossopharyngeal)?

A
  • Hypersensitive carotid sinus reflex
  • Loss of gag reflex (afferent)

These signs indicate dysfunction of the glossopharyngeal nerve.

359
Q

What is the clinical pathway for Nerve IX (Glossopharyngeal)?

A

Jugular foramen

This is the foramen through which the glossopharyngeal nerve exits the skull.

360
Q

What are the functions of Nerve X (Vagus)?

A
  • Phonation
  • Swallowing
  • Innervates viscera

Vagus nerve has extensive autonomic functions throughout the body.

361
Q

What lesions may occur with Nerve X (Vagus)?

A
  • Uvula deviates away from site of lesion
  • Loss of gag reflex (efferent)

These signs indicate dysfunction of the vagus nerve.

362
Q

What is the clinical pathway for Nerve X (Vagus)?

A

Jugular foramen

This is the foramen through which the vagus nerve exits the skull.

363
Q

What is the function of Nerve XI (Accessory)?

A

Head and shoulder movement

Accessory nerve innervates muscles that control head and shoulder movements.

364
Q

What lesions may occur with Nerve XI (Accessory)?

A
  • Weakness turning head to contralateral side

This indicates dysfunction of the accessory nerve.

365
Q

What is the clinical pathway for Nerve XI (Accessory)?

A

Jugular foramen

This is the foramen through which the accessory nerve exits the skull.

366
Q

What is the function of Nerve XII (Hypoglossal)?

A

Tongue movement

Hypoglossal nerve controls the movements of the tongue.

367
Q

What is a clinical sign of a palsy in Nerve XII (Hypoglossal)?

A

Tongue deviates towards side of lesion

This indicates weakness in the muscles on one side of the tongue.

368
Q

What is the clinical pathway for Nerve XII (Hypoglossal)?

A

Hypoglossal canal

This is the foramen through which the hypoglossal nerve exits the skull.

369
Q

Mnemonic for cranial nerves - ?sensory or motor

A

Some Say Marry Money But My Brother Says Big Brains Matter Most

S = Sensory, M = Motor, B = Both

372
Q

Who should diagnose and manage Parkinson’s disease?

A

A specialist with expertise in movement disorders

373
Q

What is the first-line treatment if motor symptoms affect quality of life?

374
Q

What is the first-line treatment if motor symptoms do not affect quality of life?

A

Dopamine agonist (non-ergot derived), levodopa or MAO-B inhibitor

375
Q

What are the benefits of Levodopa in treating Parkinson’s?

A
  • More improvement in motor symptoms
  • More improvement in activities of daily living
  • Fewer specified adverse events (e.g., excessive sleepiness, hallucinations, impulse control disorders)
376
Q

What are the downsides of Levodopa?

A
  • More motor complications
377
Q

How does dopamine agonists compare to Levodopa and other drugs ?

A
  • Less improvement in motor symptoms compared to Levodopa but compared to others has improvement
  • Less improvement in activities of daily living compared to Levodopa but compared to others has improvement
  • Fewer motor complications
  • More off-time reduction compared to COMT/MAO-B/Amantidine
  • More specified adverse events compared to Levodopa, Intermediate risk of adverse events compared to COMT/MAO-B/Amantidine
  • More risk of hallucinations
378
Q

What are the effects of MAO-B inhibitors?

A
  • Less improvement in motor symptoms compared to Levodopa but compared to others has improvement
  • Less improvement in activities of daily living compared to Levodopa but compared to others has improvement
  • Fewer motor complications
  • Has off-time reduction
  • Fewer specified adverse events compared to Levodopa and COMT/MAO-B/Amantidine
    *Lower risk of hallucinations
379
Q

What is the effect of COMT inhibitors?

A

Improvement in motor symptoms
Improvement in ADLs
Off time reduction
More adverse events
Lower risk of hallucinations

380
Q

What are the adverse effects of COMT inhibitors?

A

More adverse events

381
Q

What is the evidence regarding Amantidine’s effects?

A
  • No evidence for motor symptoms
  • No evidence for activities of daily living
  • No studies for off time
  • No studies for adverse effects
382
Q

What does NICE recommend if a patient continues to have symptoms despite optimal levodopa treatment?

A

Addition of a dopamine agonist, MAO-B inhibitor or COMT inhibitor as an adjunct

383
Q

Fill in the blank: a patient continues to have symptoms despite optimal levodopa or If a patient has developed dyskinesia, NICE recommends the addition of a _______ as an adjunct.

A

dopamine agonist, MAO-B inhibitor or COMT inhibitor

384
Q

True or False: Levodopa has fewer motor complications than dopamine agonists.

386
Q

What is the risk associated with not taking Parkinson’s medication?

A

Acute akinesia or neuroleptic malignant syndrome

This can occur if medication is not absorbed, for example, due to gastroenteritis.

387
Q

What should be avoided in Parkinson’s patients regarding medication?

A

‘Drug holiday’

It is advised against due to the risk of acute akinesia or neuroleptic malignant syndrome.

388
Q

What are the common causes of impulse control disorders in Parkinson’s patients?

A
  • Dopamine agonist therapy
  • History of previous impulsive behaviors
  • History of alcohol consumption and/or smoking

These disorders have become a significant issue in recent years.

389
Q

What should patients with excessive daytime sleepiness refrain from doing?

A

Driving

Medication should be adjusted to control symptoms.

390
Q

What medication can be considered if alternative strategies fail for excessive daytime sleepiness?

391
Q

What should be done if orthostatic hypotension develops in Parkinson’s patients?

A

Medication review

If symptoms persist, midodrine can be considered.

392
Q

What is the role of glycopyrronium bromide in Parkinson’s disease?

A

To manage drooling of saliva.

393
Q

What is levodopa commonly combined with?

A

Decarboxylase inhibitor (e.g. carbidopa or benserazide)

This combination prevents peripheral metabolism of levodopa to dopamine outside of the brain.

394
Q

What are common adverse effects of levodopa?

A
  • Dry mouth
  • Anorexia
  • Palpitations
  • Postural hypotension
  • Psychosis

Some adverse effects are due to the difficulty in achieving a steady dose.

395
Q

What is the ‘end-of-dose wearing off’ phenomenon?

A

Symptoms worsen towards the end of the dosage interval.

396
Q

What describes the ‘on-off’ phenomenon in Parkinson’s medication?

A

Large variations in motor performance, normal function during ‘on’ period, weakness during ‘off’ period.

397
Q

What are dyskinesias at peak dose in Parkinson’s patients?

A

Dystonia, chorea, and athetosis (involuntary writhing movements).

398
Q

What should not be done acutely with levodopa?

A

Stop levodopa.

399
Q

What can be given as rescue medication if a patient cannot take levodopa orally?

A

Dopamine agonist patch.

400
Q

Name some dopamine receptor agonists used in Parkinson’s treatment.

A
  • Bromocriptine
  • Ropinirole
  • Cabergoline
  • Apomorphine

Ergot-derived dopamine receptor agonists have specific side effects.

401
Q

What are potential complications of ergot-derived dopamine receptor agonists?

A
  • Pulmonary fibrosis
  • Retroperitoneal fibrosis
  • Cardiac fibrosis

Patients should be monitored closely and screened prior to treatment.

402
Q

What is the effect of MAO-B inhibitors like selegiline?

A

Inhibits the breakdown of dopamine.

403
Q

What is the mechanism of action of Amantadine?

A

Probably increases dopamine release and inhibits its uptake at dopaminergic synapses.

404
Q

What are the side effects of Amantadine?

A
  • Ataxia
  • Slurred speech
  • Confusion
  • Dizziness
  • Livedo reticularis
405
Q

What is the role of COMT inhibitors like entacapone and tolcapone?

A

Used as an adjunct to levodopa therapy.

406
Q

What is the purpose of antimuscarinics in Parkinson’s treatment?

A

Block cholinergic receptors to help tremor and rigidity.

407
Q

Name examples of antimuscarinics used to treat drug induced Parkinson’s.

A
  • Procyclidine
  • Benzotropine
  • Trihexyphenidyl (benzhexol)

Now used more for drug-induced parkinsonism than idiopathic Parkinson’s disease.

408
Q

What is the most common cause of dementia in the UK?

A

The most common cause of dementia in the UK is Alzheimer’s disease, followed by vascular dementia and Lewy body dementia. These conditions may coexist.

409
Q

What are the common causes of dementia?

A

Common causes include Alzheimer’s disease, cerebrovascular disease (multi-infarct dementia), and Lewy body dementia.

410
Q

What are the rarer causes of dementia?

A

Rarer causes of dementia include Huntington’s disease, CJD, Pick’s disease, and HIV (in 50% of AIDS patients).

411
Q

What assessment tools are recommended by NICE for non-specialist settings?

A

Recommended tools include the 10-point cognitive screener (10-CS) and the 6-Item cognitive impairment test (6CIT).

412
Q

What assessment tools are not recommended by NICE for non-specialist settings?

A

Not recommended tools include the abbreviated mental test score (AMTS), general practitioner assessment of cognition (GPCOG), and the mini-mental state examination (MMSE).

413
Q

What blood tests does NICE recommend in primary care to exclude reversible causes of dementia?

A

NICE recommends FBC, U&E, LFTs, calcium, glucose, ESR/CRP, TFTs, vitamin B12, and folate levels.

414
Q

What is performed in secondary care to exclude reversible conditions in dementia patients?

A

Neuroimaging is performed to exclude other reversible conditions and to provide information on aetiology, guiding prognosis and management.

415
Q

What should be offered according to the 2018 NICE guidelines for dementia diagnosis?

A

Structural imaging should be offered to help exclude reversible causes of cognitive decline and assist with subtype diagnosis unless dementia is well established.

416
Q

Who commonly leads memory clinics for dementia patients?

A

Memory clinics are often led by old-age psychiatrists or geriatricians.

417
Q

What is Alzheimer’s disease (AD)?

A

Alzheimer’s disease is a progressive degenerative disease of the brain accounting for the majority of dementia seen in the UK.

418
Q

What are the risk factors for Alzheimer’s disease?

A

Risk factors include increasing age, family history, inherited traits, mutations in specific genes, apoprotein E allele E4, Caucasian ethnicity, and Down’s syndrome.

419
Q

What are the macroscopic and microscopic pathological changes in Alzheimer’s disease?

A

Macroscopic changes include widespread cerebral atrophy. Microscopic changes include cortical plaques and neurofibrillary tangles.

420
Q

What is the biochemical change associated with Alzheimer’s disease?

A

There is a deficit of acetylcholine from damage to an ascending forebrain projection.

421
Q

What is the role of tau protein in Alzheimer’s disease?

A

In Alzheimer’s disease, tau proteins are excessively phosphorylated, impairing their function.

422
Q

What non-pharmacological management does NICE recommend for Alzheimer’s disease?

A

NICE recommends offering a range of activities to promote wellbeing tailored to the person’s preference and group cognitive stimulation therapy.

423
Q

What pharmacological treatments are recommended for mild to moderate Alzheimer’s disease?

A

The three acetylcholinesterase inhibitors (donepezil, galantamine, rivastigmine) are recommended.

424
Q

What is memantine’s role in Alzheimer’s disease management?

A

Memantine is a second-line treatment for moderate Alzheimer’s, used when patients are intolerant of acetylcholinesterase inhibitors or as an add-on for moderate or severe Alzheimer’s.

425
Q

What does NICE say about managing non-cognitive symptoms in dementia?

A

NICE does not recommend antidepressants for mild to moderate depression and advises using antipsychotics only for severe distress.

426
Q

What are the contraindications and adverse effects of donepezil?

A

Donepezil is relatively contraindicated in patients with bradycardia, and adverse effects include insomnia.

427
Q

What is Lewy body dementia?

A

An increasingly recognised cause of dementia, accounting for up to 20% of cases

Characterized by alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas.

428
Q

What is the characteristic pathological feature of Lewy body dementia?

A

Alpha-synuclein cytoplasmic inclusions (Lewy bodies)

Found in the substantia nigra, paralimbic, and neocortical areas.

429
Q

How is Lewy body dementia related to Parkinson’s disease?

A

The relationship is complicated; dementia is often seen in Parkinson’s disease

Up to 40% of patients with Alzheimer’s have Lewy bodies.

430
Q

What are the main features of Lewy body dementia?

A

Progressive cognitive impairment, parkinsonism, visual hallucinations

Early impairments in attention and executive function rather than just memory loss.

431
Q

What is the typical progression of symptoms in Lewy body dementia?

A

Cognitive impairment typically occurs before parkinsonism

Both features usually occur within a year of each other.

432
Q

How does cognition in Lewy body dementia differ from other forms of dementia?

A

Cognition may be fluctuating

In contrast to Alzheimer’s, where memory loss is more prominent.

433
Q

What visual symptoms are associated with Lewy body dementia?

A

Visual hallucinations, delusions, and non-visual hallucinations

These symptoms may also be present.

434
Q

What is the typical method of diagnosis for Lewy body dementia?

A

Usually clinical, with SPECT increasingly used

SPECT is commercially known as a DaTscan.

435
Q

What is the sensitivity and specificity of SPECT in diagnosing Lewy body dementia?

A

Sensitivity is around 90%, specificity is 100%

Uses dopaminergic iodine-123-radiolabelled 2-carbomethoxy-3-(4-iodophenyl)-N-(3-fluoropropyl) nortropane (123-I FP-CIT) as the radioisotope.

436
Q

What medications can be used to manage Lewy body dementia?

A

Acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine

Similar to treatments used in Alzheimer’s.

437
Q

What should be avoided in the management of Lewy body dementia?

A

Neuroleptics

Patients are extremely sensitive and may develop irreversible parkinsonism.

438
Q

True or False: In Lewy body dementia, motor symptoms typically present at least one year before cognitive symptoms.

A

False

In Lewy body dementia, cognitive impairment typically occurs before motor symptoms.

439
Q

Fill in the blank: The characteristic inclusions found in Lewy body dementia are called _______.

A

Lewy bodies

These inclusions are primarily composed of alpha-synuclein.

440
Q

What is frontotemporal lobar degeneration (FTLD)?

A

The third most common type of cortical dementia after Alzheimer’s and Lewy body dementia.

FTLD is characterized by various clinical presentations and is distinguished from other types of dementia.

441
Q

What are the three recognized types of FTLD?

A
  • Frontotemporal dementia (Pick’s disease)
  • Progressive non fluent aphasia (chronic progressive aphasia, CPA)
  • Semantic dementia

Each type has distinct clinical features and symptoms.

442
Q

What are common features of frontotemporal lobar dementias?

A
  • Onset before 65
  • Insidious onset
  • Relatively preserved memory and visuospatial skills
  • Personality change and social conduct problems

These features help differentiate FTLD from other dementias.

443
Q

What characterizes Pick’s disease?

A

Personality change and impaired social conduct, along with hyperorality, disinhibition, increased appetite, and perseveration behaviours.

Pick’s disease is the most common type of FTLD.

444
Q

What is a characteristic macroscopic change seen in Pick’s disease?

A

Atrophy of the frontal and temporal lobes.

This atrophy contributes to the symptoms observed in patients.

445
Q

What is a characteristic microscopic change in Pick’s disease?

A
  • Pick bodies - spherical aggregations of tau protein (silver-staining)
  • Gliosis
  • Neurofibrillary tangles
  • Senile plaques

These microscopic features are critical for diagnosis.

446
Q

What is the management recommendation for AChE inhibitors or memantine in frontotemporal dementia?

A

NICE do not recommend their use in people with frontotemporal dementia.

This reflects the limited efficacy of these treatments in FTLD.

447
Q

What is the chief factor in progressive non fluent aphasia (CPA)?

A

Non fluent speech characterized by short utterances that are agrammatic.

Comprehension remains relatively preserved in CPA.

448
Q

What is a key feature of semantic dementia?

A

Fluent progressive aphasia where speech is fluent but empty and conveys little meaning.

Unlike in Alzheimer’s, memory is better for recent rather than remote events.

449
Q

What does left homonymous hemianopia indicate?

A

Visual field defect to the left due to lesion of right optic tract

Left homonymous hemianopia results in loss of vision in the left visual field.

450
Q

What are homonymous quadrantanopias and what is the mnemonic used to remember their locations?

A

PITS (Parietal-Inferior, Temporal-Superior)

Homonymous quadrantanopias refer to quadrant-specific visual field defects based on the location of the lesion.

451
Q

What is the difference between congruous and incongruous defects?

A

Congruous defects are complete or symmetrical visual field loss; incongruous defects are incomplete or asymmetric.

Congruous defects indicate a lesion in the optic radiation or occipital cortex, while incongruous defects indicate a lesion in the optic tract.

452
Q

What type of lesion causes incongruous defects?

A

Lesion of optic tract

Incongruous defects indicate that the visual field loss is not symmetrical.

453
Q

What type of lesion is associated with congruous defects?

A

Lesion of optic radiation or occipital cortex

Congruous defects reflect a more complete and symmetrical loss of vision.

454
Q

What does macula sparing indicate?

A

Lesion of occipital cortex

Macula sparing refers to preservation of central vision despite visual field loss.

455
Q

What is the cause of superior homonymous quadrantanopia?

A

Lesion of the inferior optic radiations in the temporal lobe (Meyer’s loop)

This type of defect results in loss of vision in the upper quadrant of the visual field.

456
Q

What causes inferior homonymous quadrantanopia?

A

Lesion of the superior optic radiations in the parietal lobe

This results in loss of vision in the lower quadrant of the visual field.

457
Q

What is bitemporal hemianopia and what causes it?

A

Lesion of optic chiasm

Bitemporal hemianopia results in loss of vision in the outer (temporal) fields of both eyes.

458
Q

What visual field defect is associated with inferior chiasmal compression?

A

Upper quadrant defect > lower quadrant defect

This condition is commonly associated with a pituitary tumor.

459
Q

What visual field defect is associated with superior chiasmal compression?

A

Lower quadrant defect > upper quadrant defect

This condition is commonly associated with a craniopharyngioma.

460
Q

What is the general characteristic of most seizures?

A

Most seizures are self-limiting and stop spontaneously.

461
Q

What is a potential risk associated with prolonged seizures?

A

Prolonged seizures may be potentially life-threatening.

462
Q

What is the first step in the acute management of seizures?

A

Check the airway and apply oxygen if appropriate.

463
Q

What position should a patient be placed in after a seizure?

A

Place the patient in the recovery position.

464
Q

What should be administered if a seizure is prolonged?

A

Give benzodiazepines.

465
Q

What is the recommended dose for rectal diazepam in neonates for acute seizure?

A

1.25 - 2.5 mg.

466
Q

What is the recommended dose for rectal diazepam for children aged 1 month - 1 year for acute seizure?

467
Q

What is the recommended dose for rectal diazepam for children aged 2 years - 11 years for acute seziure?

A

5 - 10 mg.

468
Q

What is the recommended dose for rectal diazepam for children aged 12 years - 17 years acute seizure?

469
Q

What is the recommended dose for rectal diazepam for adults acute seizure?

A

10 - 20 mg (max. 30 mg).

470
Q

What is the recommended dose for rectal diazepam for the elderly acute seizure ?

A

10 mg (max. 15 mg).

471
Q

What alternative medication may be used for acute seizure management?

A

Midazolam oromucosal solution.

472
Q

What is the dose of midazolam oromucosal solution for neonates acute seizures ?

A

300 mcg/kg (unlicensed).

473
Q

What is the maximum dose of midazolam for children aged 1 - 2 months acute seizure ?

A

300 mcg/kg (max. 2.5 mg, unlicensed).

474
Q

What is the recommended dose for midazolam for children aged 3 - 11 months acute seizures ?

475
Q

What is the recommended dose for midazolam for children aged 1 - 4 years acute seizure ?

476
Q

What is the recommended dose for midazolam for children aged 5 - 9 years acute seizure ?

477
Q

What is the recommended dose for midazolam for children aged 10 - 17 years acute seizure ?

478
Q

What is the recommended dose for midazolam for adults acute seizures ?

A

10 mg (unlicensed).

480
Q

What is the recommended adrenaline dose for infants under 6 months?

A

100 - 150 micrograms (0.1 - 0.15 ml 1 in 1,000)

Doses are critical for effective anaphylaxis management.

481
Q

What is the recommended adrenaline dose for children aged 6 months to 6 years?

A

150 micrograms (0.15 ml 1 in 1,000)

Accurate dosing is essential for safety and efficacy.

482
Q

What is the recommended adrenaline dose for children aged 6-12 years?

A

300 micrograms (0.3 ml 1 in 1,000)

Dosing varies with age and weight.

483
Q

What is the recommended adrenaline dose for adults and children over 12 years?

A

500 micrograms (0.5 ml 1 in 1,000)

Adult dosing reflects greater body mass and potential severity.

484
Q

How often can adrenaline be repeated in an anaphylaxis case?

A

Every 5 minutes if necessary

Timely administration can be life-saving.

485
Q

What is the best site for IM injection of adrenaline?

A

Anterolateral aspect of the middle third of the thigh

Proper injection technique is crucial for absorption.

486
Q

What defines refractory anaphylaxis?

A

Respiratory and/or cardiovascular problems persist despite 2 doses of IM adrenaline

Indicates a severe, ongoing reaction requiring further intervention.

487
Q

What should be given for shock in refractory anaphylaxis?

A

IV fluids

Fluid resuscitation is important for stabilizing the patient.

488
Q

What should be sought in cases of refractory anaphylaxis?

A

Expert help for consideration of an IV adrenaline infusion

Advanced care may be necessary for severe cases.

489
Q

What type of antihistamines may be given after initial stabilization?

A

Non-sedating oral antihistamines

Preferable to chlorphenamine, especially for skin symptoms.

490
Q

What is a potential challenge in diagnosing anaphylaxis?

A

Establishing whether a patient had a true episode of anaphylaxis

Diagnosis can be complicated and may require serum tryptase levels.

491
Q

How long can serum tryptase levels remain elevated after an acute episode of anaphylaxis?

A

Up to 12 hours

Useful for confirming anaphylaxis diagnosis.

492
Q

What should all patients with a new diagnosis of anaphylaxis be referred to?

A

A specialist allergy clinic

Ongoing management and education are essential.

493
Q

What interim measure should be given before a specialist allergy assessment?

A

An adrenaline injector

Important for patient safety until further evaluation.

494
Q

How many adrenaline auto-injectors should patients be prescribed?

A

2 adrenaline auto-injectors

Ensures availability in case of multiple reactions.

495
Q

What training should be provided to patients prescribed adrenaline auto-injectors?

A

Training on how to use the injector

Proper use is critical for effectiveness.

496
Q

What is the risk of biphasic reactions in patients with anaphylaxis?

A

Can occur in up to 20% of patients

Monitoring post-discharge is important.

497
Q

What is required for fast-track discharge after anaphylaxis?

A

Good response to a single dose of adrenaline, complete resolution of symptoms, given an adrenaline auto-injector, adequate supervision

Fast-tracking is based on clinical stability.

498
Q

What is the minimum observation time after symptom resolution for patients needing 2 doses of IM adrenaline?

A

6 hours

Extended observation is critical for safety.

499
Q

What conditions require a minimum of 12 hours observation after symptom resolution?

A

Severe reaction requiring > 2 doses of IM adrenaline, patient has severe asthma, possibility of ongoing reaction, presents late at night, difficult access to emergency care

These factors increase risk for complications.