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AKT 3 Flashcards

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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
What is the incubation period for Salmonella and Escherichia coli?
12-48 hours
26
What is the incubation period for Shigella and Campylobacter?
48-72 hours
27
What is the incubation period for Giardiasis and Amoebiasis?
> 7 days
28
What is a Fibroadenoma?
Common in women under the age of 30 years, described as 'breast mice' due to being discrete, non-tender, highly mobile lumps ## Footnote Fibroadenomas are benign breast tumors that are often found in young women.
29
What is Fibroadenosis also known as?
Fibrocystic disease, benign mammary dysplasia ## Footnote This condition is characterized by 'lumpy' breasts which may be painful, with symptoms worsening prior to menstruation.
30
What are the characteristic features of breast cancer?
Hard, irregular lump; may have associated nipple inversion or skin tethering ## Footnote Early detection is crucial for better outcomes in breast cancer treatment.
31
What is Paget's disease of the breast?
Intraductal carcinoma associated with reddening and thickening of the nipple/areola, resembling eczematous changes ## Footnote This condition can indicate underlying breast cancer.
32
What is Mammary duct ectasia?
Dilatation of the large breast ducts, most common around menopause ## Footnote May present with a tender lump around the areola and green nipple discharge; if ruptured, can cause local inflammation.
33
What is a Duct papilloma?
Local areas of epithelial proliferation in large mammary ducts, hyperplastic lesions rather than malignant or premalignant ## Footnote May present with blood-stained discharge.
34
What is Fat necrosis?
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 ## Footnote This condition is rare and can mimic breast cancer, warranting further investigation.
35
What is a Breast abscess?
More common in lactating women; characterized by red, hot tender swelling ## Footnote Prompt treatment is necessary to manage abscesses effectively.
36
Fill in the blank: Lipomas and _______ may also develop around the breast tissue.
sebaceous cysts ## Footnote These are generally benign conditions that can occur in breast tissue.
37
What is required for patients taking antipsychotic medication?
Extensive monitoring in addition to clinical follow-up ## Footnote The monitoring includes various health factors that need to be measured regularly.
38
What factors need to be measured when on antipsychotics?
* Full blood count (FBC) * Urea and electrolytes (U&E) * Liver function tests (LFT) * Lipids * Fasting glucose * Prolactin * Weight * Blood pressure * ECG * Qrisk/cardiovascular assessment ## Footnote These factors are critical for ensuring the safety and effectiveness of antipsychotic treatment.
39
When should FBC, U&E, and LFT be measured for antipsychotic therapy?
At the start of therapy and annually ## Footnote These tests are crucial for monitoring potential side effects of antipsychotic medications.
40
How often does clozapine require monitoring of FBC?
Initially weekly ## Footnote Clozapine has a higher risk of agranulocytosis, necessitating more frequent monitoring.
41
When should lipids and weight be measured during antipsychotic therapy?
At the start of therapy, at 3 months, and annually ## Footnote Monitoring these factors helps assess metabolic side effects of antipsychotics.
42
When should fasting blood glucose and prolactin be measured?
At the start of therapy, at 6 months, and annually ## Footnote This monitoring is important to detect metabolic changes and hormonal effects.
43
When should blood pressure be monitored during antipsychotic therapy?
Baseline and frequently during dose titration ## Footnote Blood pressure monitoring is essential to manage potential cardiovascular risks.
44
When should an electrocardiogram (ECG) be performed?
At baseline ## Footnote An ECG helps identify any pre-existing cardiac issues before starting treatment.
45
How often should cardiovascular risk assessment be conducted?
Annually ## Footnote This assessment is crucial for patients on antipsychotics to manage long-term health risks.
46
When should clozapine be introduced in the treatment of schizophrenia?
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.
47
What is the incidence of agranulocytosis with clozapine?
1%
48
What is the incidence of neutropaenia with clozapine?
3%
49
What effect does clozapine have on seizure threshold?
It can reduce seizure threshold and induce seizures in up to 3% of patients.
50
List some adverse effects of clozapine.
* Agranulocytosis * Neutropaenia * Reduced seizure threshold * Constipation * Myocarditis * Hypersalivation
51
What should be done before starting treatment with clozapine?
A baseline ECG should be taken.
52
What might necessitate a dose adjustment of clozapine?
If smoking is started or stopped during treatment.
53
What is lithium used for in psychiatric treatment?
Prophylaxis in bipolar disorder and adjunct in refractory depression ## Footnote Lithium is primarily used to stabilize mood in bipolar disorder patients and can also help those with treatment-resistant depression.
54
What is the therapeutic range for lithium?
0.4-1.0 mmol/L ## Footnote This narrow therapeutic range means careful monitoring is essential to avoid toxicity.
55
What is the primary route of excretion for lithium?
Kidneys ## Footnote Lithium is primarily excreted unchanged in the urine, necessitating renal function monitoring.
56
What are the two theories regarding lithium's mechanism of action?
* Interferes with inositol triphosphate formation * Interferes with cAMP formation ## Footnote The exact mechanism remains unclear, but these theories suggest how lithium may influence neurotransmitter signaling.
57
List some common adverse effects of lithium.
* Nausea/vomiting * Diarrhoea * Fine tremor * Nephrotoxicity * Thyroid enlargement * ECG changes * Weight gain * Idiopathic intracranial hypertension * Leucocytosis * Hyperparathyroidism ## Footnote These adverse effects require monitoring and may necessitate adjustments in treatment.
58
What is a specific renal adverse effect associated with lithium?
Nephrogenic diabetes insipidus ## Footnote This condition leads to polyuria and can significantly affect fluid balance.
59
When should lithium levels be checked after starting therapy?
Weekly and after each dose change until stable ## Footnote Regular monitoring is crucial to ensure therapeutic effectiveness and safety.
60
How often should lithium blood levels be checked once established?
Every 3 months ## Footnote Consistent monitoring helps prevent toxicity and manage therapeutic levels.
61
What additional monitoring is required for patients on lithium?
* Thyroid function every 6 months * Renal function every 6 months ## Footnote Due to the potential for thyroid and renal adverse effects, regular assessments are necessary.
62
What patient education materials should be provided to those on lithium therapy?
* Information booklet * Alert card * Record book ## Footnote These materials help patients understand their treatment and the importance of monitoring.
63
True or False: Lithium has a long plasma half-life.
True ## Footnote This characteristic affects dosing intervals and monitoring requirements.
64
Fill in the blank: Lithium levels should be taken _______ hours post-dose.
12 ## Footnote Timing of blood draws is critical for accurate measurement of lithium levels.
65
What ECG changes may occur with lithium use?
T wave flattening/inversion ## Footnote These changes can indicate cardiac effects of lithium therapy.
66
What blood tests are required for monitoring patients on Statins?
LFTs at baseline, 3 months, and 12 months ## Footnote LFTs refer to Liver Function Tests.
67
What blood tests must be done prior to treatment with ACE inhibitors?
U&E prior to treatment ## Footnote U&E refers to Urea and Electrolytes.
68
How often should U&E be monitored for patients on ACE inhibitors after increasing the dose?
U&E after increasing dose and at least annually
69
What tests are required prior to treatment with Amiodarone?
TFT, LFT, U&E, CXR prior to treatment ## Footnote CXR refers to Chest X-Ray.
70
How frequently should TFT and LFT be monitored for patients on Amiodarone?
Every 6 months
71
What tests are required for monitoring patients on Methotrexate?
FBC, LFT, U&E ## Footnote FBC refers to Full Blood Count.
72
What is the monitoring recommendation for FBC and renal and LFTs before starting Methotrexate?
FBC and renal and LFTs before starting treatment and repeated weekly until therapy stabilised, thereafter every 2-3 months
73
What tests should be done before treatment with Azathioprine?
FBC, LFT before treatment
74
How often should FBC be monitored for the first 4 weeks of Azathioprine treatment?
Weekly for the first 4 weeks
75
What is the monitoring schedule for FBC and LFT for patients on Azathioprine after the first 4 weeks?
Every 3 months
76
What tests are required prior to treatment with Lithium?
Lithium level, TFT, U&E
77
How often should Lithium levels be monitored until stabilized?
Weekly until stabilised
78
What is the monitoring schedule for TFT and U&E for patients on Lithium?
Every 6 months
79
What tests should be done before treatment with Sodium Valproate?
LFT, FBC before treatment
80
How often should LFT be monitored during the first 6 months of Sodium Valproate treatment?
Periodically
81
What tests are required before treatment with Glitazones?
LFT before treatment
82
How often should LFT be monitored during treatment with Glitazones?
Regularly
83
What is a common feature of Patau syndrome (trisomy 13)?
Microcephalic, small eyes ## Footnote Other features include cleft lip/palate, polydactyly, and scalp lesions.
84
What are typical characteristics of Edward's syndrome (trisomy 18)?
Micrognathia, low-set ears, rocker bottom feet, overlapping of fingers ## Footnote These features are often used for diagnosis.
85
What are the main symptoms of Fragile X syndrome?
Learning difficulties, macrocephaly, long face, large ears, macro-orchidism ## Footnote Fragile X is the most common inherited cause of intellectual disability.
86
Which features are associated with Noonan syndrome?
Webbed neck, pectus excavatum, short stature, pulmonary stenosis ## Footnote Noonan syndrome can present with various congenital heart defects.
87
What are the defining characteristics of Pierre-Robin syndrome?
Micrognathia, posterior displacement of the tongue, cleft palate ## Footnote The posterior tongue displacement may result in upper airway obstruction.
88
List the features of Prader-Willi syndrome.
Hypotonia, hypogonadism, obesity ## Footnote This syndrome is known for its insatiable appetite leading to obesity.
89
What features are commonly seen in William's syndrome?
Short stature, learning difficulties, friendly extrovert personality, transient neonatal hypercalcaemia, supravalvular aortic stenosis ## Footnote Individuals often have a distinctive facial appearance.
90
What is a characteristic cry associated with Cri du chat syndrome?
Characteristic cry due to larynx and neurological problems ## Footnote Other features include feeding difficulties, learning difficulties, and microcephaly.
91
True or False: Treacher-Collins syndrome is autosomal recessive.
False ## Footnote Treacher-Collins syndrome is autosomal dominant, often with a family history.
92
Fill in the blank: Cri du chat syndrome is caused by a _______ on chromosome 5p.
deletion ## Footnote This deletion leads to the various features associated with the syndrome.
93
What is Turner's syndrome?
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.
94
What is the chromosomal notation for Turner's syndrome?
45,XO or 45,X
95
List three physical features commonly associated with Turner's syndrome.
* Short stature * Shield chest, widely spaced nipples * Webbed neck
96
What are two serious long-term health problems for women with Turner's syndrome?
* Aortic dilatation * Aortic dissection
97
Why is regular monitoring important in adult life for women with Turner's syndrome?
To check for complications related to aortic dilatation and dissection.
98
What is primary amenorrhoea?
The absence of menstrual periods in women with Turner's syndrome.
99
What is cystic hygroma, and when is it often diagnosed?
A fluid-filled sac often diagnosed prenatally.
100
What is a common dental feature in individuals with Turner's syndrome?
High-arched palate
101
What skeletal abnormality is often seen in Turner's syndrome?
Short fourth metacarpal
102
What is the most common renal abnormality in Turner's syndrome?
Horseshoe kidney
103
What are gonadotrophin levels like in individuals with Turner's syndrome?
Elevated
104
What endocrine disorder is much more common in Turner's syndrome?
Hypothyroidism
105
True or False: There is an increased incidence of autoimmune disease in Turner's syndrome.
True
106
Name an autoimmune disease that has a higher incidence in Turner's syndrome.
Autoimmune thyroiditis
107
What gastrointestinal condition is more common in individuals with Turner's syndrome?
Crohn's disease
108
What percentage of individuals with Turner's syndrome have a bicuspid aortic valve?
15%
109
What percentage of individuals with Turner's syndrome may have coarctation of the aorta?
5-10%
110
What condition can cause lymphoedema in neonates with Turner's syndrome?
Lymphoedema, especially in the feet
111
Fill in the blank: Turner's syndrome is a chromosomal disorder affecting around 1 in ______ females.
2,500
112
What is the LH and testosterone level in primary hypogonadism (Klinefelter's syndrome)?
LH: High, Testosterone: Low
113
What are the LH and testosterone levels in hypogonadotrophic hypogonadism (Kallman's syndrome)?
LH: Low, Testosterone: Low
114
What are the LH and testosterone levels in androgen insensitivity syndrome?
LH: High, Testosterone: Normal/high
115
What is the LH and testosterone level in testosterone-secreting tumour?
LH: Low, Testosterone: High
116
What is the karyotype associated with Klinefelter's syndrome?
47, XXY
117
List the features of Klinefelter's syndrome.
* Often taller than average * Lack of secondary sexual characteristics * Small, firm testes * Infertile * Gynaecomastia * Elevated gonadotrophin levels
118
How is Klinefelter's syndrome diagnosed?
By chromosomal analysis
119
What causes Kallman's syndrome?
Failure of GnRH-secreting neurons to migrate to the hypothalamus
120
What key symptom is associated with Kallman's syndrome?
Lack of smell (anosmia)
121
List the features of Kallman's syndrome.
* Delayed puberty * Hypogonadism * Cryptorchidism * Anosmia * Low sex hormone levels * Inappropriately low/normal LH, FSH levels * Typically normal or above average height
122
What additional defects may be seen in some patients with Kallman's syndrome?
* Cleft lip/palate * Visual/hearing defects
123
What is the genetic basis of androgen insensitivity syndrome?
X-linked recessive condition
124
What is the phenotype of genotypically male children with androgen insensitivity syndrome?
Female phenotype
125
What is the new term for testicular feminisation syndrome?
Complete androgen insensitivity syndrome
126
List the features of androgen insensitivity syndrome.
* Primary amenorrhea * Undescended testes * Groin swellings * Breast development due to conversion of testosterone to oestradiol
127
How is androgen insensitivity syndrome diagnosed?
Buccal smear or chromosomal analysis to reveal 46XY genotype
128
What is the management approach for androgen insensitivity syndrome?
* Counselling to raise child as female * Bilateral orchidectomy * Oestrogen therapy
129
What is the most common malignancy in men aged 20-30 years?
Testicular cancer ## Footnote Testicular cancer primarily affects younger men, highlighting the importance of awareness and early detection.
130
What percentage of testicular cancer cases are germ-cell tumours?
Around 95% ## Footnote Germ-cell tumours are the predominant form of testicular cancer.
131
What are the two main categories of germ cell tumours?
Seminomas and non-seminomas ## Footnote Non-seminomas include embryonal, yolk sac, teratoma, and choriocarcinoma.
132
Name two types of non-germ cell tumours.
* Leydig cell tumours * Sarcomas ## Footnote Non-germ cell tumours represent a different classification than germ cell tumours.
133
At what age is the peak incidence for teratomas?
25 years ## Footnote Understanding peak incidence helps in identifying at-risk populations.
134
At what age is the peak incidence for seminomas?
35 years ## Footnote This age distribution is crucial for screening and awareness.
135
What are some risk factors for testicular cancer?
* Infertility (increases risk by a factor of 3) * Cryptorchidism * Family history * Klinefelter's syndrome * Mumps orchitis ## Footnote Knowledge of these risk factors can aid in early detection and management.
136
What is the most common presenting symptom of testicular cancer?
A painless lump ## Footnote Early recognition of symptoms can lead to timely diagnosis.
137
What additional symptoms may occur in a minority of men with testicular cancer?
* Pain * Hydrocele * Gynaecomastia ## Footnote These symptoms can vary and may indicate underlying pathology.
138
What hormonal changes contribute to gynaecomastia in testicular cancer?
Increased oestrogen:androgen ratio ## Footnote This hormonal imbalance is significant in the pathophysiology of testicular cancer.
139
What is the elevation of hCG in seminomas?
May be elevated in around 20% ## Footnote This is important for diagnosis and monitoring treatment response.
140
What tumour markers are elevated in non-seminomas?
AFP and/or beta-hCG in 80-85% ## Footnote These markers are critical for identifying and managing non-seminomatous germ cell tumours.
141
What is the first-line diagnostic tool for testicular cancer?
Ultrasound ## Footnote Ultrasound is a non-invasive method essential for initial evaluation.
142
What are the primary management options for testicular cancer?
* Orchidectomy * Chemotherapy * Radiotherapy ## Footnote Management strategies depend on the type and stage of the tumour.
143
What is the 5-year survival rate for seminomas at Stage I?
Around 95% ## Footnote This high survival rate underscores the effectiveness of early treatment.
144
What is the 5-year survival rate for teratomas at Stage I?
Around 85% ## Footnote The prognosis remains favorable with early intervention.
145
What type of conditions are often thought to be 'metabolic'?
Autosomal recessive conditions ## Footnote This contrasts with autosomal dominant conditions which are often considered 'structural'.
146
Provide an example of an X-linked recessive metabolic condition.
Hunter's syndrome ## Footnote Another example is G6PD deficiency.
147
Which conditions are notable exceptions to the classification of metabolic and structural?
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. ## Footnote This highlights the complexity in classifying genetic conditions.
148
List three autosomal recessive conditions.
* Albinism * Ataxic telangiectasia * Congenital adrenal hyperplasia
149
Which autosomal recessive condition is characterized by thick, sticky mucus production?
Cystic fibrosis ## Footnote This condition affects the lungs and digestive system.
150
What is Friedreich's ataxia classified as?
Autosomal recessive ## Footnote It is a genetic condition that affects the nervous system and the heart.
151
Fill in the blank: Gilbert's syndrome is still a matter of debate and many textbooks will list it as _______ dominant.
autosomal
152
Name a condition associated with lipid storage disorders that is autosomal recessive.
Tay-Sach's ## Footnote Other examples include Gaucher and Niemann-Pick diseases.
153
Which autosomal recessive condition is characterized by the body’s inability to process phenylalanine?
PKU ## Footnote PKU stands for phenylketonuria.
154
True or False: Sickle cell anemia is an autosomal recessive condition.
True
155
What is the classification of Wilson's disease?
Autosomal recessive ## Footnote This condition leads to excessive copper accumulation in the body.
156
List two conditions that can cause periodic paralysis and are classified as autosomal dominant.
* Hyperlipidemia type II * Hypokalemic periodic paralysis
157
What is the genetic classification of Familial Mediterranean Fever?
Autosomal recessive
158
What type of inheritance pattern does Haemochromatosis follow?
Autosomal recessive ## Footnote This condition leads to excessive iron absorption in the body.
159
Fill in the blank: The condition known as Cystinuria is classified as _______ recessive.
autosomal
160
What is the classification of Glycogen storage disease?
Autosomal recessive
161
What type of inheritance do conditions like Achondroplasia have?
Autosomal dominant
162
Name a condition that is classified as autosomal dominant.
Achondroplasia
163
Name a condition associated with autosomal dominant inheritance that affects the skin and connective tissue.
Ehlers-Danlos syndrome
164
Which autosomal dominant condition is characterized by the presence of multiple colon polyps?
Familial adenomatous polyposis
165
What is the inheritance pattern of Huntington's disease?
Autosomal dominant
166
True or False: Neurofibromatosis is an autosomal dominant condition.
True
167
Fill in the blank: _______ syndrome is an autosomal dominant condition that affects connective tissues.
Marfan's
168
What is the inheritance pattern of Von Willebrand's disease type 3?
Autosomal recessive
169
List three conditions that are autosomal dominant.
* Acute intermittent porphyria * Myotonic dystrophy * Retinoblastoma
170
Which autosomal dominant condition is associated with a deficiency of Antithrombin III?
Antithrombin III deficiency
171
What is the relationship between hereditary haemorrhagic telangiectasia and inheritance?
It is autosomal dominant
172
Fill in the blank: _______ syndrome is associated with an increased risk of developing colorectal cancer and is inherited in an autosomal dominant manner.
Hereditary non-polyposis colorectal carcinoma
173
Name an autosomal dominant condition that can lead to malignant hyperthermia.
Malignant hyperthermia
174
True or False: Osteogenesis imperfecta is an autosomal dominant condition.
True
175
What type of inheritance does Peutz-Jeghers syndrome follow?
Autosomal dominant
176
List two conditions that are classified as autosomal dominant.
* Hyperlipidaemia type II * Noonan syndrome
177
Which autosomal dominant condition is characterized by the formation of tumors in the nervous system?
Neurofibromatosis
178
Fill in the blank: _______ syndrome is a genetic disorder characterized by the development of tumors and is inherited in an autosomal dominant pattern.
Tuberous sclerosis
179
What is a common feature of many autosomal dominant conditions?
They often manifest in individuals with only one copy of the mutated gene.
180
What conditions do not require school exclusion?
Conjunctivitis, Fifth disease (slapped cheek), Roseola, Infectious mononucleosis, Head lice, Threadworms, Hand, foot and mouth ## Footnote These conditions are generally not contagious enough to warrant exclusion from school.
181
How long after commencing antibiotics for scarlet fever should a child be excluded from school?
24 hours ## Footnote This is to ensure that the child is no longer contagious.
182
What is the exclusion period for whooping cough?
2 days after commencing antibiotics or 21 days from onset of symptoms if no antibiotics ## Footnote This ensures that the risk of transmission is minimized.
183
How many days after the onset of rash should a child with measles be excluded?
4 days from onset of rash ## Footnote This is to prevent the spread of the virus in schools.
184
What is the exclusion period for rubella?
5 days from onset of rash ## Footnote This helps limit the risk of infection to others.
185
When can a child return to school after chickenpox?
All lesions crusted over or 5 days after the onset of rash ## Footnote It's important to ensure that the child is no longer infectious.
186
What is the exclusion period for mumps?
5 days from onset of swollen glands ## Footnote This time frame is necessary to reduce the risk of spreading the virus.
187
How long should a child be excluded if they have diarrhea and vomiting?
Until symptoms have settled for 48 hours ## Footnote This is to prevent the spread of infectious agents.
188
What is the exclusion requirement for impetigo?
Until lesions are crusted and healed, or 48 hours after commencing antibiotic treatment ## Footnote This ensures the child is no longer contagious.
189
What should be done for a child with scabies regarding school exclusion?
Until treated ## Footnote This is crucial to prevent further spread of scabies.
190
When can a child return to school after influenza?
Until recovered ## Footnote This helps ensure that the child is fit to participate in school activities.
191
True or False: Chickenpox is infectious from 2 days before the rash appears to 5 days after the onset of rash.
True ## Footnote This highlights the contagious nature of chickenpox.
192
What vaccine is given at birth if risk factors are present?
BCG vaccine ## Footnote Given if there are risk factors for tuberculosis, such as a family history in the past 6 months.
193
What does the '6-1 vaccine' include?
* Diphtheria * Tetanus * Whooping cough * Polio * Hib * Hepatitis B ## Footnote Administered at 2, 3, and 4 months.
194
At what age is the oral rotavirus vaccine administered?
2 months and 3 months ## Footnote It is part of the vaccination schedule for infants.
195
What vaccine is given at 3 months alongside the '6-1 vaccine'?
PCV ## Footnote Pneumococcal conjugate vaccine.
196
What vaccines are administered at 12-13 months?
* Hib/Men C * MMR * PCV * Men B ## Footnote These vaccines are crucial for early childhood health.
197
What is the annual vaccine given between 2-8 years?
Flu vaccine ## Footnote Administered annually to protect against influenza.
198
What does the '4-in-1 pre-school booster' include?
* Diphtheria * Tetanus * Whooping cough * Polio ## Footnote Given at 3-4 years of age.
199
At what age is the HPV vaccination administered?
12-13 years ## Footnote Human papillomavirus vaccination.
200
What does the '3-in-1 teenage booster' include?
* Tetanus * Diphtheria * Polio ## Footnote Given between 13-18 years.
201
What vaccine has replaced meningitis C for 13-18 year-olds?
Meningitis ACWY vaccine ## Footnote Due to an increased incidence of meningitis W disease.
202
Who is advised to get the Men ACWY vaccine?
* 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 ## Footnote Students should contact their GP to receive the vaccine ideally before the academic year starts.
203
What should be done for children with severe or life-threatening asthma?
Transfer immediately to hospital
204
What is the SpO2 level indicative of a moderate asthma attack in children aged 2 to 5 years?
SpO2 > 92%
205
List the clinical features of a severe asthma attack in children aged 2 to 5 years.
* SpO2 < 92% * Too breathless to talk or feed * Heart rate > 140/min * Respiratory rate > 40/min * Use of accessory neck muscles
206
What defines a life-threatening asthma attack in children aged 2 to 5 years?
* SpO2 < 92% * Silent chest * Poor respiratory effort * Agitation * Altered consciousness * Cyanosis
207
What should be attempted to measure in children greater than 5 years of age during an asthma attack?
PEF (Peak Expiratory Flow)
208
What is the SpO2 level indicative of a moderate asthma attack in children greater than 5 years?
SpO2 > 92%
209
What are the clinical features of a severe asthma attack in children greater than 5 years?
* 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
What defines a life-threatening asthma attack in children greater than 5 years?
* SpO2 < 92% * PEF < 33% best or predicted * Silent chest * Poor respiratory effort * Altered consciousness * Cyanosis
211
What is the first line of treatment for children with mild to moderate acute asthma?
Bronchodilator therapy
212
How should a beta-2 agonist be administered to children with mild to moderate acute asthma?
Via a spacer (close-fitting mask for children < 3 years), 1 puff every 30-60 seconds up to a maximum of 10 puffs
213
What should be done if symptoms are not controlled after administering a beta-2 agonist?
Repeat beta-2 agonist and refer to hospital
214
What type of therapy should be given to all children with an asthma exacerbation?
Steroid therapy
215
What is the duration of steroid treatment for children with asthma exacerbation?
3-5 days
216
What is the usual prednisolone dose for children aged 2-5 years?
20 mg od/1-2 mg/kg od (max 40mg)
217
What is the usual prednisolone dose for children greater than 5 years?
30 - 40 mg od/1-2 mg/kg od (max 40mg)
218
What method should be used to measure temperature in children less than 4 weeks old?
An electronic thermometer in the axilla ## Footnote This method is recommended for accurate temperature measurement in very young infants.
219
What types of thermometers can be used for measuring temperature in children older than 4 weeks?
Electronic/chemical dot thermometer in the axilla or an infra-red tympanic thermometer ## Footnote These thermometers provide alternative methods for temperature measurement in older children.
220
What does the green traffic light indicate for fever in children?
Low risk ## Footnote Normal colour, responds normally to social cues, normal circulation and hydration
221
What are the signs of the green category?
• Normal colour • Responds normally to social cues • Strong normal cry/not crying • Normal skin and eyes • Moist mucous membranes • No amber or red signs ## Footnote These indicate a low risk for serious illness.
222
What does the amber traffic light indicate for fever in children?
Intermediate risk ## Footnote Signs include pallor and decreased responsiveness.
223
What are the signs of the amber category?
• 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 ## Footnote Specific age and temperature criteria also apply.
224
What respiratory signs indicate a child is in the amber category?
• Nasal flaring • Respiratory rate >50 breaths/minute (age 6-12 months) • Respiratory rate >40 breaths/minute (age >12 months) ## Footnote These signs suggest a moderate risk of serious illness.
225
What is the tachycardia threshold for children under 12 months in the amber category?
>160 beats/minute ## Footnote Tachycardia thresholds vary by age.
226
What does the red traffic light indicate for fever in children?
High risk ## Footnote Immediate medical attention is required.
227
What are the signs of the red category?
• 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 ## Footnote These signs indicate a severe and potentially life-threatening condition.
228
What should be done if a child is categorized as amber?
Provide parents with a safety net or refer to a paediatric specialist ## Footnote Safety net includes information on warning symptoms and how to access further healthcare.
229
What should be done if a child is categorized as red?
Refer child urgently to a paediatric specialist ## Footnote Immediate action is critical for high-risk indicators.
230
True or False: Oral antibiotics should be prescribed to children with fever without apparent source.
False ## Footnote Antibiotics should not be prescribed without a clear source of infection.
231
If pneumonia is suspected but the child is not referred to hospital, what is the protocol regarding chest x-rays?
A chest x-ray does not need to be routinely performed ## Footnote This applies only if the child is not being referred.
232
What is the prevalence of headache in boys and girls before puberty?
Equally as common in boys and girls until puberty, then a strong (3:1) female preponderance.
233
What is the most common cause of primary headache in children?
Migraine without aura.
234
What are the criteria for pediatric migraine without aura according to the International Headache Society?
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
What is the preferred acute management medication for pediatric migraine?
Ibuprofen is thought to be more effective than paracetamol.
236
At what age can triptans be used for children, and what is the only licensed triptan with proven efficacy?
Triptans may be used in children >= 12 years; sumatriptan nasal spray is licensed.
237
What are some side effects of triptans?
* Tingling * Heat * Heaviness/pressure sensations
238
What is the status of oral triptans for individuals under 18 years?
Oral triptans are not currently licensed in people < 18 years.
239
What are the first-line preventative treatments for pediatric migraine according to the GOSH website?
* Pizotifen * Propranolol
240
What are the second-line preventative treatments for pediatric migraine?
* Valproate * Topiramate * Amitryptiline
241
What is the second most common cause of headache in children?
Tension-type headache (TTH).
242
What are the diagnostic criteria for tension-type headache in children?
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
What is the function of the trabecular network?
It offers increased resistance to aqueous outflow, causing increased IOP.
244
What is the aim of treatment for increased intra-ocular pressure (IOP)?
To lower intra-ocular pressure to prevent progressive loss of visual field.
245
What does NICE guidelines recommend as first-line treatment for IOP of ≥ 24 mmHg?
360° selective laser trabeculoplasty (SLT).
246
What are the benefits of 360° SLT?
It can delay the need for eye drops and reduce but not eliminate the chance they will be needed.
247
What may be needed at a later date after the first 360° SLT procedure?
A second 360° SLT procedure.
248
What are the second-line treatments according to NICE?
Prostaglandin analogue (PGA) eyedrops.
249
List the next line of treatments for increased IOP.
* Beta-blocker eye drops * Carbonic anhydrase inhibitor eye drops * Sympathomimetic eye drops * Surgery (trabeculectomy) in refractory cases.
250
What is the action of prostaglandin analogues (e.g. latanoprost)?
Increases uveoscleral outflow with once daily administration.
251
What are the adverse effects of prostaglandin analogues?
* Brown pigmentation of the iris * Increased eyelash length.
252
What is the effect of beta-blockers (e.g. timolol, betaxolol) on aqueous production?
Reduces aqueous production.
253
Who should avoid beta-blockers?
Asthmatics and patients with heart block.
254
What is the action of sympathomimetics (e.g. brimonidine)?
Reduces aqueous production and increases outflow.
255
What should be avoided when taking sympathomimetics?
MAOI or tricyclic antidepressants.
256
What are the adverse effects of sympathomimetics?
Hyperaemia.
257
What is the action of carbonic anhydrase inhibitors (e.g. Dorzolamide)?
Reduces aqueous production.
258
What adverse reactions may occur due to systemic absorption of carbonic anhydrase inhibitors?
Sulphonamide-like reactions.
259
What is the action of miotics (e.g. pilocarpine)?
Increases uveoscleral outflow.
260
What is a direct parasympathomimetic used to treat Acute glaucoma?
Pilocarpine ## Footnote Pilocarpine causes contraction of the ciliary muscle, leading to the opening of the trabecular meshwork and increased outflow of aqueous humour.
261
What is the mechanism of action of beta-blockers in treating Acute glaucoma?
Decreases aqueous humour production ## Footnote An example of a beta-blocker used is timolol.
262
What is an alpha-2 agonist used in the treatment of Acute glaucoma?
Apraclonidine ## Footnote Apraclonidine has a dual mechanism of decreasing aqueous humour production and increasing uveoscleral outflow.
263
What is the role of intravenous acetazolamide in treating Acute glaucoma?
Reduces aqueous secretions ## Footnote It is used to lower intraocular pressure in acute situations.
264
What is recommended alongside other treatments to reduce inflammation in Acute glaucoma?
Topical steroids ## Footnote Some guidelines suggest using topical steroids as part of the management plan.
265
What is the definitive management procedure for Acute glaucoma?
Laser peripheral iridotomy ## Footnote This procedure creates a tiny hole in the peripheral iris to allow aqueous humour to flow to the angle.
266
Fill in the blank: A direct parasympathomimetic like _______ causes contraction of the ciliary muscle.
pilocarpine
267
True or False: Timolol is an alpha-2 agonist used in the treatment of Acute glaucoma.
False ## Footnote Timolol is a beta-blocker, while apraclonidine is the alpha-2 agonist.
268
What is the driving rule for hypertension?
Can drive unless treatment causes unacceptable side effects; no need to notify DVLA. ## Footnote If Group 2 Entitlement, disqualified from driving if resting BP consistently 180 mmHg systolic or more and/or 100 mmHg diastolic or more.
269
What is the required off-driving period after elective angioplasty?
1 week off driving.
270
How long must a patient refrain from driving after CABG?
4 weeks off driving.
271
What is the driving restriction duration for acute coronary syndrome?
4 weeks off driving; 1 week if successfully treated by angioplasty.
272
When must driving cease for a patient with angina?
If symptoms occur at rest or at the wheel.
273
What is the off-driving period after pacemaker insertion?
1 week off driving.
274
What are the driving rules for an implantable cardioverter-defibrillator (ICD)?
Cease driving for 6 months if implanted for sustained ventricular arrhythmia; 1 month if implanted prophylactically. Permanent bar for Group 2 drivers.
275
How long must a patient refrain from driving after successful catheter ablation for an arrhythmia?
2 days off driving.
276
What should patients with an aortic aneurysm of 6 cm or more do?
Notify DVLA; licensing permitted subject to annual review.
277
What is the driving restriction for an aortic diameter of 6.5 cm or more?
Disqualifies patients from driving.
278
What is the driving rule after a heart transplant?
Do not drive for 6 weeks; no need to notify DVLA.
279
What should all patients with epilepsy/seizures do regarding driving?
Must not drive and must inform the DVLA ## Footnote This includes all types of seizures.
280
What is the driving restriction period after a first unprovoked/isolated seizure without relevant abnormalities?
6 months off driving ## Footnote If there are structural abnormalities or epileptiform activity, the period increases to 12 months.
281
What is the driving qualification condition for patients with established epilepsy?
Must be free from any seizure for 12 months ## Footnote A 'til 70 licence can be restored if there have been no seizures for 5 years.
282
What should patients do while withdrawing from epilepsy medication?
Should not drive during withdrawal and for 6 months after last dose ## Footnote This ensures safety during a sensitive period.
283
What is the driving restriction for a simple faint?
No restriction ## Footnote Simple fainting does not typically affect driving ability.
284
What is the driving restriction for a single episode of syncope that is unexplained?
6 months off driving ## Footnote This is to ensure safety while the cause is investigated.
285
What is the driving restriction for two or more episodes of syncope?
12 months off driving ## Footnote Multiple episodes indicate a higher risk of recurrence.
286
What is the driving restriction after a stroke or TIA if there is no residual neurological deficit?
1 month off driving ## Footnote May not need to inform the DVLA in this case.
287
What is the driving restriction after multiple TIAs over a short period?
3 months off driving and inform DVLA ## Footnote This is due to increased risk of driving impairment.
288
What is the driving restriction after a craniotomy for a meningioma?
1 year off driving ## Footnote If the tumour is benign and no seizure history, reconsideration may be possible after 6 months.
289
What is the driving restriction after a pituitary tumour craniotomy?
6 months off driving ## Footnote Patients can drive when there is no residual impairment affecting safe driving.
290
What should patients with narcolepsy/cataplexy do regarding driving?
Cease driving on diagnosis and can restart once symptoms are under satisfactory control ## Footnote This is essential for safety on the road.
291
What should be done by patients with chronic neurological disorders like multiple sclerosis?
Inform the DVLA and complete the PK1 form ## Footnote This is necessary to assess their fitness to drive.
292
What condition was previously restricted from holding a HGV licence until October 2011?
diabetes mellitus ## Footnote The DVLA changed the rules regarding HGV licences for individuals with diabetes.
293
What are the standards that must be met for a driver with diabetes on insulin to hold a HGV licence?
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 ## Footnote These standards also apply to patients using other hypoglycaemic inducing drugs.
294
What form must insulin-using patients complete to apply for a Group 2 (HGV) licence?
VDIAB1I form ## Footnote This form is specifically for patients on insulin who want to apply for a HGV licence.
295
What conditions allow a patient on insulin to drive a car?
Conditions include: * Hypoglycaemic awareness * No more than one episode of hypoglycaemia requiring assistance in the last 12 months * No relevant visual impairment ## Footnote Drivers are usually contacted by the DVLA.
296
Do drivers taking tablets or exenatide need to notify the DVLA?
No, unless the tablets may induce hypoglycaemia ## Footnote In such cases, they must not have experienced more than one episode requiring assistance in the last 12 months.
297
What is the requirement for drivers whose diabetes is controlled by diet alone?
No requirement to inform DVLA ## Footnote This applies to individuals managing their diabetes strictly through dietary measures.
298
How often must blood glucose monitoring be conducted to demonstrate adequate control for HGV licence applicants?
At least twice daily ## Footnote This includes monitoring at times relevant to driving.
299
What additional feature should blood glucose meters have for applicants to demonstrate adequate control?
Memory function ## Footnote Applicants should have used these meters for at least 3 months prior to application.
300
What are the rules for individuals with severe anxiety or depression regarding driving?
Must not drive and must notify the DVLA ## Footnote Applies if there are significant memory problems, concentration problems, agitation, behavioral disturbance, or suicidal thoughts.
301
What is required for individuals experiencing acute psychotic disorder?
Must not drive during acute illness and must notify the DVLA ## Footnote This applies during the period of acute illness.
302
What are the driving regulations for individuals with hypomania or mania?
Must not drive during acute illness and must notify the DVLA ## Footnote This rule is in place during the acute phase of the condition.
303
What should individuals with schizophrenia do regarding driving?
Must not drive during acute illness and must notify the DVLA ## Footnote This is required during the acute phase of the illness.
304
Can individuals with pervasive developmental disorders and ADHD drive?
May be able to drive but must inform the DVLA ## Footnote Notification to the DVLA is necessary in this case.
305
What is the driving status for individuals with mild cognitive impairment?
May drive and need not inform the DVLA ## Footnote This condition does not require notification.
306
What must individuals with dementia do regarding driving?
May be able to drive but must inform the DVLA ## Footnote It is important to notify the DVLA.
307
What are the driving regulations for individuals with mild learning disability?
May be able to drive but must inform the DVLA ## Footnote Notification to the DVLA is required.
308
What is the driving status for individuals with severe disability?
Must not drive and must notify the DVLA ## Footnote This applies to those with significant impairments.
309
Can individuals with personality disorders drive?
May be able to drive but must inform the DVLA ## Footnote It is necessary to notify the DVLA about their condition.
310
What is the minimum period required for licence revocation or refusal due to persistent alcohol misuse?
6 months of controlled drinking or abstinence with normalisation of blood parameters ## Footnote Persistent alcohol misuse is confirmed by medical enquiry and/or abnormal blood markers.
311
How long is the licence revocation period for alcohol dependency?
1 year ## Footnote This is in line with the guidelines for persistent alcohol misuse.
312
What substances lead to a minimum 6 month licence refusal or revocation if there is persistent use or dependency?
* Cannabis * Amphetamines * Ecstasy * LSD ## Footnote Medical enquiry confirmation is required for these substances.
313
What is the minimum period for licence refusal or revocation for heroin, cocaine, or methadone dependency?
1 year ## Footnote A consultant report may be required upon reapplication.
314
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.
False ## Footnote The rules for heavy goods vehicles tend to be much stricter.
315
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 _______.
dependency ## Footnote This definition highlights the potential harm caused by alcohol misuse.
316
What must drivers with visual field defects do?
Driving must cease unless confirmed able to meet recommended national guidelines for visual field ## Footnote This ensures safety on the road due to potential limitations in vision.
317
What is required of drivers with monocular vision?
Must notify DVLA ## Footnote They may drive if acuity and visual field is normal in the remaining eye.
318
What should a driver with blepharospasm seek?
Consultant opinion is required ## Footnote This is necessary to assess their ability to drive safely.
319
Which drivers have stricter rules according to the DVLA guidelines?
Drivers of heavy goods vehicles ## Footnote These drivers are subject to more stringent regulations due to the nature of their vehicles.
320
What are the three classifications of diabetic retinopathy?
Non-proliferative diabetic retinopathy (NPDR), proliferative retinopathy (PDR), maculopathy ## Footnote These classifications help in assessing the severity and treatment options for diabetic retinopathy.
321
What characterizes Mild Non-proliferative diabetic retinopathy (NPDR)?
1 or more microaneurysm ## Footnote Mild NPDR indicates the earliest stage of diabetic retinopathy.
322
List the features of Moderate Non-proliferative diabetic retinopathy (NPDR).
* microaneurysms * blot haemorrhages * hard exudates * cotton wool spots * venous beading/looping * intraretinal microvascular abnormalities (IRMA) less severe than in severe NPDR ## Footnote Moderate NPDR shows more significant changes in the retina.
323
What defines Severe Non-proliferative diabetic retinopathy (NPDR)?
* blot haemorrhages and microaneurysms in 4 quadrants * venous beading in at least 2 quadrants * IRMA in at least 1 quadrant ## Footnote Severe NPDR indicates a high risk of progression to proliferative diabetic retinopathy.
324
What are the key features of Proliferative diabetic retinopathy (PDR)?
* retinal neovascularisation * fibrous tissue forming anterior to retinal disc * more common in Type I DM * 50% blind in 5 years ## Footnote PDR is a more advanced stage of diabetic retinopathy with significant risk of vision loss.
325
What is maculopathy based on?
Location rather than severity ## Footnote Maculopathy can be serious regardless of the severity of other changes in the retina.
326
What are the key features of maculopathy?
* hard exudates * other 'background' changes on macula * check visual acuity * more common in Type II DM ## Footnote Maculopathy focuses on the macula, which is crucial for central vision.
327
What is the general management approach for all diabetic retinopathy patients?
* optimise glycaemic control * manage blood pressure * control hyperlipidemia * regular review by ophthalmology ## Footnote Effective management can slow the progression of diabetic retinopathy.
328
What treatment is indicated for maculopathy if there is a change in visual acuity?
Intravitreal vascular endothelial growth factor (VEGF) inhibitors ## Footnote These inhibitors can help improve visual outcomes in patients with maculopathy.
329
What is recommended for Non-proliferative retinopathy management?
Regular observation ## Footnote Severe or very severe cases may require panretinal laser photocoagulation.
330
What is the treatment for Proliferative retinopathy?
* panretinal laser photocoagulation * intravitreal VEGF inhibitors * vitreoretinal surgery if severe or vitreous haemorrhage ## Footnote These treatments aim to prevent vision loss and manage complications.
331
True or False: Following treatment for proliferative retinopathy, around 50% of patients develop a noticeable reduction in their visual fields.
True ## Footnote This reduction is due to the scarring of peripheral retinal tissue.
332
What are some complications of proliferative retinopathy treatments?
* decrease in night vision * generalised decrease in visual acuity * macular oedema ## Footnote Night vision is primarily affected due to the role of rod cells in low light conditions.
333
Fill in the blank: Examples of intravitreal VEGF inhibitors include _______.
ranibizumab ## Footnote These medications are often used alongside laser treatments.
334
What is the role of intravitreal VEGF inhibitors in the treatment of proliferative diabetic retinopathy?
They slow progression and improve visual acuity ## Footnote Combining these inhibitors with laser treatment enhances patient outcomes.
335
What is the function of Nerve I (Olfactory)?
Smell ## Footnote Nerve I is responsible for the sense of smell.
336
What is the clinical pathway for Nerve I (Olfactory)?
Cribriform plate ## Footnote This is the structure through which the olfactory nerve fibers pass.
337
What is the function of Nerve II (Optic)?
Sight ## Footnote Nerve II is responsible for vision.
338
What is the clinical pathway for Nerve II (Optic)?
Optic canal ## Footnote This is the passage through which the optic nerve travels.
339
What are the functions of Nerve III (Oculomotor)?
- Eye movement (MR, IO, SR, IR) - Pupil constriction - Accommodation - Eyelid opening ## Footnote MR: Medial Rectus, IO: Inferior Oblique, SR: Superior Rectus, IR: Inferior Rectus.
340
What are the clinical signs of a palsy in Nerve III (Oculomotor)?
- Ptosis 'down and out' eye - Dilated, fixed pupil ## Footnote These symptoms indicate dysfunction of the oculomotor nerve.
341
What is the clinical pathway for Nerve III (Oculomotor)?
Superior orbital fissure (SOF) ## Footnote This is the foramen through which the oculomotor nerve exits the skull.
342
What is the function of Nerve IV (Trochlear)?
Eye movement (SO) ## Footnote Trochlear nerve is primarily responsible for the movement of the superior oblique muscle.
343
What is a clinical sign of a palsy in Nerve IV (Trochlear)?
Defective downward gaze → vertical diplopia ## Footnote Vertical diplopia occurs when the eyes are not properly aligned.
344
What is the clinical pathway for Nerve IV (Trochlear)?
Superior orbital fissure (SOF) ## Footnote This is the foramen through which the trochlear nerve travels.
345
What are the functions of Nerve V (Trigeminal)?
- Facial sensation - Mastication ## Footnote Trigeminal nerve has three branches: V1, V2, and V3.
346
What lesions may occur with Nerve V (Trigeminal)?
- Trigeminal neuralgia - Loss of corneal reflex (afferent) - Loss of facial sensation - Paralysis of mastication muscles - Deviation of jaw to weak side ## Footnote These are common clinical manifestations related to trigeminal nerve lesions.
347
What is the clinical pathway for Nerve V (Trigeminal)?
V1: SOF, V2: Foramen rotundum, V3: Foramen ovale ## Footnote Each branch of the trigeminal nerve exits the skull through different foramina.
348
What is the function of Nerve VI (Abducens)?
Eye movement (LR) ## Footnote Abducens nerve controls the lateral rectus muscle.
349
What is a clinical sign of a palsy in Nerve VI (Abducens)?
Defective abduction → horizontal diplopia ## Footnote Horizontal diplopia occurs when the eyes fail to move laterally properly.
350
What is the clinical pathway for Nerve VI (Abducens)?
Superior orbital fissure (SOF) ## Footnote This is the foramen through which the abducens nerve exits the skull.
351
What are the functions of Nerve VII (Facial)?
- Facial movement - Taste (anterior 2/3rds of tongue) - Lacrimation - Salivation ## Footnote Facial nerve controls muscles of facial expression and taste sensations.
352
What lesions may occur with Nerve VII (Facial)?
- Flaccid paralysis of upper + lower face - Loss of corneal reflex (efferent) - Loss of taste - Hyperacusis ## Footnote These signs indicate dysfunction of the facial nerve.
353
What is the clinical pathway for Nerve VII (Facial)?
Internal auditory meatus ## Footnote This is the structure through which the facial nerve exits the skull.
354
What are the functions of Nerve VIII (Vestibulocochlear)?
- Hearing - Balance ## Footnote Vestibulocochlear nerve is responsible for auditory and vestibular functions.
355
What lesions may occur with Nerve VIII (Vestibulocochlear)?
- Hearing loss - Vertigo - Nystagmus - Acoustic neuromas ## Footnote These conditions are associated with vestibulocochlear nerve dysfunction.
356
What is the clinical pathway for Nerve VIII (Vestibulocochlear)?
Internal auditory meatus ## Footnote This is the foramen through which the vestibulocochlear nerve exits the skull.
357
What are the functions of Nerve IX (Glossopharyngeal)?
- Taste (posterior 1/3rd of tongue) - Salivation - Swallowing - Mediates input from carotid body & sinus ## Footnote Glossopharyngeal nerve is involved in taste and autonomic functions.
358
What lesions may occur with Nerve IX (Glossopharyngeal)?
- Hypersensitive carotid sinus reflex - Loss of gag reflex (afferent) ## Footnote These signs indicate dysfunction of the glossopharyngeal nerve.
359
What is the clinical pathway for Nerve IX (Glossopharyngeal)?
Jugular foramen ## Footnote This is the foramen through which the glossopharyngeal nerve exits the skull.
360
What are the functions of Nerve X (Vagus)?
- Phonation - Swallowing - Innervates viscera ## Footnote Vagus nerve has extensive autonomic functions throughout the body.
361
What lesions may occur with Nerve X (Vagus)?
- Uvula deviates away from site of lesion - Loss of gag reflex (efferent) ## Footnote These signs indicate dysfunction of the vagus nerve.
362
What is the clinical pathway for Nerve X (Vagus)?
Jugular foramen ## Footnote This is the foramen through which the vagus nerve exits the skull.
363
What is the function of Nerve XI (Accessory)?
Head and shoulder movement ## Footnote Accessory nerve innervates muscles that control head and shoulder movements.
364
What lesions may occur with Nerve XI (Accessory)?
- Weakness turning head to contralateral side ## Footnote This indicates dysfunction of the accessory nerve.
365
What is the clinical pathway for Nerve XI (Accessory)?
Jugular foramen ## Footnote This is the foramen through which the accessory nerve exits the skull.
366
What is the function of Nerve XII (Hypoglossal)?
Tongue movement ## Footnote Hypoglossal nerve controls the movements of the tongue.
367
What is a clinical sign of a palsy in Nerve XII (Hypoglossal)?
Tongue deviates towards side of lesion ## Footnote This indicates weakness in the muscles on one side of the tongue.
368
What is the clinical pathway for Nerve XII (Hypoglossal)?
Hypoglossal canal ## Footnote This is the foramen through which the hypoglossal nerve exits the skull.
369
Mnemonic for cranial nerves - ?sensory or motor
Some Say Marry Money But My Brother Says Big Brains Matter Most S = Sensory, M = Motor, B = Both
370
371
372
Who should diagnose and manage Parkinson's disease?
A specialist with expertise in movement disorders
373
What is the first-line treatment if motor symptoms affect quality of life?
Levodopa
374
What is the first-line treatment if motor symptoms do not affect quality of life?
Dopamine agonist (non-ergot derived), levodopa or MAO-B inhibitor
375
What are the benefits of Levodopa in treating Parkinson's?
* 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
What are the downsides of Levodopa?
* More motor complications
377
How does dopamine agonists compare to Levodopa and other drugs ?
* 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
What are the effects of MAO-B inhibitors?
* 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
What is the effect of COMT inhibitors?
Improvement in motor symptoms Improvement in ADLs Off time reduction More adverse events Lower risk of hallucinations
380
What are the adverse effects of COMT inhibitors?
More adverse events
381
What is the evidence regarding Amantidine's effects?
* No evidence for motor symptoms * No evidence for activities of daily living * No studies for off time * No studies for adverse effects
382
What does NICE recommend if a patient continues to have symptoms despite optimal levodopa treatment?
Addition of a dopamine agonist, MAO-B inhibitor or COMT inhibitor as an adjunct
383
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.
dopamine agonist, MAO-B inhibitor or COMT inhibitor
384
True or False: Levodopa has fewer motor complications than dopamine agonists.
False
385
386
What is the risk associated with not taking Parkinson's medication?
Acute akinesia or neuroleptic malignant syndrome ## Footnote This can occur if medication is not absorbed, for example, due to gastroenteritis.
387
What should be avoided in Parkinson's patients regarding medication?
'Drug holiday' ## Footnote It is advised against due to the risk of acute akinesia or neuroleptic malignant syndrome.
388
What are the common causes of impulse control disorders in Parkinson's patients?
* Dopamine agonist therapy * History of previous impulsive behaviors * History of alcohol consumption and/or smoking ## Footnote These disorders have become a significant issue in recent years.
389
What should patients with excessive daytime sleepiness refrain from doing?
Driving ## Footnote Medication should be adjusted to control symptoms.
390
What medication can be considered if alternative strategies fail for excessive daytime sleepiness?
Modafinil
391
What should be done if orthostatic hypotension develops in Parkinson's patients?
Medication review ## Footnote If symptoms persist, midodrine can be considered.
392
What is the role of glycopyrronium bromide in Parkinson's disease?
To manage drooling of saliva.
393
What is levodopa commonly combined with?
Decarboxylase inhibitor (e.g. carbidopa or benserazide) ## Footnote This combination prevents peripheral metabolism of levodopa to dopamine outside of the brain.
394
What are common adverse effects of levodopa?
* Dry mouth * Anorexia * Palpitations * Postural hypotension * Psychosis ## Footnote Some adverse effects are due to the difficulty in achieving a steady dose.
395
What is the 'end-of-dose wearing off' phenomenon?
Symptoms worsen towards the end of the dosage interval.
396
What describes the 'on-off' phenomenon in Parkinson's medication?
Large variations in motor performance, normal function during 'on' period, weakness during 'off' period.
397
What are dyskinesias at peak dose in Parkinson's patients?
Dystonia, chorea, and athetosis (involuntary writhing movements).
398
What should not be done acutely with levodopa?
Stop levodopa.
399
What can be given as rescue medication if a patient cannot take levodopa orally?
Dopamine agonist patch.
400
Name some dopamine receptor agonists used in Parkinson's treatment.
* Bromocriptine * Ropinirole * Cabergoline * Apomorphine ## Footnote Ergot-derived dopamine receptor agonists have specific side effects.
401
What are potential complications of ergot-derived dopamine receptor agonists?
* Pulmonary fibrosis * Retroperitoneal fibrosis * Cardiac fibrosis ## Footnote Patients should be monitored closely and screened prior to treatment.
402
What is the effect of MAO-B inhibitors like selegiline?
Inhibits the breakdown of dopamine.
403
What is the mechanism of action of Amantadine?
Probably increases dopamine release and inhibits its uptake at dopaminergic synapses.
404
What are the side effects of Amantadine?
* Ataxia * Slurred speech * Confusion * Dizziness * Livedo reticularis
405
What is the role of COMT inhibitors like entacapone and tolcapone?
Used as an adjunct to levodopa therapy.
406
What is the purpose of antimuscarinics in Parkinson's treatment?
Block cholinergic receptors to help tremor and rigidity.
407
Name examples of antimuscarinics used to treat drug induced Parkinson's.
* Procyclidine * Benzotropine * Trihexyphenidyl (benzhexol) ## Footnote Now used more for drug-induced parkinsonism than idiopathic Parkinson's disease.
408
What is the most common cause of dementia in the UK?
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
What are the common causes of dementia?
Common causes include Alzheimer's disease, cerebrovascular disease (multi-infarct dementia), and Lewy body dementia.
410
What are the rarer causes of dementia?
Rarer causes of dementia include Huntington's disease, CJD, Pick's disease, and HIV (in 50% of AIDS patients).
411
What assessment tools are recommended by NICE for non-specialist settings?
Recommended tools include the 10-point cognitive screener (10-CS) and the 6-Item cognitive impairment test (6CIT).
412
What assessment tools are not recommended by NICE for non-specialist settings?
Not recommended tools include the abbreviated mental test score (AMTS), general practitioner assessment of cognition (GPCOG), and the mini-mental state examination (MMSE).
413
What blood tests does NICE recommend in primary care to exclude reversible causes of dementia?
NICE recommends FBC, U&E, LFTs, calcium, glucose, ESR/CRP, TFTs, vitamin B12, and folate levels.
414
What is performed in secondary care to exclude reversible conditions in dementia patients?
Neuroimaging is performed to exclude other reversible conditions and to provide information on aetiology, guiding prognosis and management.
415
What should be offered according to the 2018 NICE guidelines for dementia diagnosis?
Structural imaging should be offered to help exclude reversible causes of cognitive decline and assist with subtype diagnosis unless dementia is well established.
416
Who commonly leads memory clinics for dementia patients?
Memory clinics are often led by old-age psychiatrists or geriatricians.
417
What is Alzheimer's disease (AD)?
Alzheimer's disease is a progressive degenerative disease of the brain accounting for the majority of dementia seen in the UK.
418
What are the risk factors for Alzheimer's disease?
Risk factors include increasing age, family history, inherited traits, mutations in specific genes, apoprotein E allele E4, Caucasian ethnicity, and Down's syndrome.
419
What are the macroscopic and microscopic pathological changes in Alzheimer's disease?
Macroscopic changes include widespread cerebral atrophy. Microscopic changes include cortical plaques and neurofibrillary tangles.
420
What is the biochemical change associated with Alzheimer's disease?
There is a deficit of acetylcholine from damage to an ascending forebrain projection.
421
What is the role of tau protein in Alzheimer's disease?
In Alzheimer's disease, tau proteins are excessively phosphorylated, impairing their function.
422
What non-pharmacological management does NICE recommend for Alzheimer's disease?
NICE recommends offering a range of activities to promote wellbeing tailored to the person's preference and group cognitive stimulation therapy.
423
What pharmacological treatments are recommended for mild to moderate Alzheimer's disease?
The three acetylcholinesterase inhibitors (donepezil, galantamine, rivastigmine) are recommended.
424
What is memantine's role in Alzheimer's disease management?
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
What does NICE say about managing non-cognitive symptoms in dementia?
NICE does not recommend antidepressants for mild to moderate depression and advises using antipsychotics only for severe distress.
426
What are the contraindications and adverse effects of donepezil?
Donepezil is relatively contraindicated in patients with bradycardia, and adverse effects include insomnia.
427
What is Lewy body dementia?
An increasingly recognised cause of dementia, accounting for up to 20% of cases ## Footnote Characterized by alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas.
428
What is the characteristic pathological feature of Lewy body dementia?
Alpha-synuclein cytoplasmic inclusions (Lewy bodies) ## Footnote Found in the substantia nigra, paralimbic, and neocortical areas.
429
How is Lewy body dementia related to Parkinson's disease?
The relationship is complicated; dementia is often seen in Parkinson's disease ## Footnote Up to 40% of patients with Alzheimer's have Lewy bodies.
430
What are the main features of Lewy body dementia?
Progressive cognitive impairment, parkinsonism, visual hallucinations ## Footnote Early impairments in attention and executive function rather than just memory loss.
431
What is the typical progression of symptoms in Lewy body dementia?
Cognitive impairment typically occurs before parkinsonism ## Footnote Both features usually occur within a year of each other.
432
How does cognition in Lewy body dementia differ from other forms of dementia?
Cognition may be fluctuating ## Footnote In contrast to Alzheimer's, where memory loss is more prominent.
433
What visual symptoms are associated with Lewy body dementia?
Visual hallucinations, delusions, and non-visual hallucinations ## Footnote These symptoms may also be present.
434
What is the typical method of diagnosis for Lewy body dementia?
Usually clinical, with SPECT increasingly used ## Footnote SPECT is commercially known as a DaTscan.
435
What is the sensitivity and specificity of SPECT in diagnosing Lewy body dementia?
Sensitivity is around 90%, specificity is 100% ## Footnote Uses dopaminergic iodine-123-radiolabelled 2-carbomethoxy-3-(4-iodophenyl)-N-(3-fluoropropyl) nortropane (123-I FP-CIT) as the radioisotope.
436
What medications can be used to manage Lewy body dementia?
Acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine ## Footnote Similar to treatments used in Alzheimer's.
437
What should be avoided in the management of Lewy body dementia?
Neuroleptics ## Footnote Patients are extremely sensitive and may develop irreversible parkinsonism.
438
True or False: In Lewy body dementia, motor symptoms typically present at least one year before cognitive symptoms.
False ## Footnote In Lewy body dementia, cognitive impairment typically occurs before motor symptoms.
439
Fill in the blank: The characteristic inclusions found in Lewy body dementia are called _______.
Lewy bodies ## Footnote These inclusions are primarily composed of alpha-synuclein.
440
What is frontotemporal lobar degeneration (FTLD)?
The third most common type of cortical dementia after Alzheimer's and Lewy body dementia. ## Footnote FTLD is characterized by various clinical presentations and is distinguished from other types of dementia.
441
What are the three recognized types of FTLD?
* Frontotemporal dementia (Pick's disease) * Progressive non fluent aphasia (chronic progressive aphasia, CPA) * Semantic dementia ## Footnote Each type has distinct clinical features and symptoms.
442
What are common features of frontotemporal lobar dementias?
* Onset before 65 * Insidious onset * Relatively preserved memory and visuospatial skills * Personality change and social conduct problems ## Footnote These features help differentiate FTLD from other dementias.
443
What characterizes Pick's disease?
Personality change and impaired social conduct, along with hyperorality, disinhibition, increased appetite, and perseveration behaviours. ## Footnote Pick's disease is the most common type of FTLD.
444
What is a characteristic macroscopic change seen in Pick's disease?
Atrophy of the frontal and temporal lobes. ## Footnote This atrophy contributes to the symptoms observed in patients.
445
What is a characteristic microscopic change in Pick's disease?
* Pick bodies - spherical aggregations of tau protein (silver-staining) * Gliosis * Neurofibrillary tangles * Senile plaques ## Footnote These microscopic features are critical for diagnosis.
446
What is the management recommendation for AChE inhibitors or memantine in frontotemporal dementia?
NICE do not recommend their use in people with frontotemporal dementia. ## Footnote This reflects the limited efficacy of these treatments in FTLD.
447
What is the chief factor in progressive non fluent aphasia (CPA)?
Non fluent speech characterized by short utterances that are agrammatic. ## Footnote Comprehension remains relatively preserved in CPA.
448
What is a key feature of semantic dementia?
Fluent progressive aphasia where speech is fluent but empty and conveys little meaning. ## Footnote Unlike in Alzheimer's, memory is better for recent rather than remote events.
449
What does left homonymous hemianopia indicate?
Visual field defect to the left due to lesion of right optic tract ## Footnote Left homonymous hemianopia results in loss of vision in the left visual field.
450
What are homonymous quadrantanopias and what is the mnemonic used to remember their locations?
PITS (Parietal-Inferior, Temporal-Superior) ## Footnote Homonymous quadrantanopias refer to quadrant-specific visual field defects based on the location of the lesion.
451
What is the difference between congruous and incongruous defects?
Congruous defects are complete or symmetrical visual field loss; incongruous defects are incomplete or asymmetric. ## Footnote Congruous defects indicate a lesion in the optic radiation or occipital cortex, while incongruous defects indicate a lesion in the optic tract.
452
What type of lesion causes incongruous defects?
Lesion of optic tract ## Footnote Incongruous defects indicate that the visual field loss is not symmetrical.
453
What type of lesion is associated with congruous defects?
Lesion of optic radiation or occipital cortex ## Footnote Congruous defects reflect a more complete and symmetrical loss of vision.
454
What does macula sparing indicate?
Lesion of occipital cortex ## Footnote Macula sparing refers to preservation of central vision despite visual field loss.
455
What is the cause of superior homonymous quadrantanopia?
Lesion of the inferior optic radiations in the temporal lobe (Meyer's loop) ## Footnote This type of defect results in loss of vision in the upper quadrant of the visual field.
456
What causes inferior homonymous quadrantanopia?
Lesion of the superior optic radiations in the parietal lobe ## Footnote This results in loss of vision in the lower quadrant of the visual field.
457
What is bitemporal hemianopia and what causes it?
Lesion of optic chiasm ## Footnote Bitemporal hemianopia results in loss of vision in the outer (temporal) fields of both eyes.
458
What visual field defect is associated with inferior chiasmal compression?
Upper quadrant defect > lower quadrant defect ## Footnote This condition is commonly associated with a pituitary tumor.
459
What visual field defect is associated with superior chiasmal compression?
Lower quadrant defect > upper quadrant defect ## Footnote This condition is commonly associated with a craniopharyngioma.
460
What is the general characteristic of most seizures?
Most seizures are self-limiting and stop spontaneously.
461
What is a potential risk associated with prolonged seizures?
Prolonged seizures may be potentially life-threatening.
462
What is the first step in the acute management of seizures?
Check the airway and apply oxygen if appropriate.
463
What position should a patient be placed in after a seizure?
Place the patient in the recovery position.
464
What should be administered if a seizure is prolonged?
Give benzodiazepines.
465
What is the recommended dose for rectal diazepam in neonates for acute seizure?
1.25 - 2.5 mg.
466
What is the recommended dose for rectal diazepam for children aged 1 month - 1 year for acute seizure?
5 mg.
467
What is the recommended dose for rectal diazepam for children aged 2 years - 11 years for acute seziure?
5 - 10 mg.
468
What is the recommended dose for rectal diazepam for children aged 12 years - 17 years acute seizure?
10 mg.
469
What is the recommended dose for rectal diazepam for adults acute seizure?
10 - 20 mg (max. 30 mg).
470
What is the recommended dose for rectal diazepam for the elderly acute seizure ?
10 mg (max. 15 mg).
471
What alternative medication may be used for acute seizure management?
Midazolam oromucosal solution.
472
What is the dose of midazolam oromucosal solution for neonates acute seizures ?
300 mcg/kg (unlicensed).
473
What is the maximum dose of midazolam for children aged 1 - 2 months acute seizure ?
300 mcg/kg (max. 2.5 mg, unlicensed).
474
What is the recommended dose for midazolam for children aged 3 - 11 months acute seizures ?
2.5 mg.
475
What is the recommended dose for midazolam for children aged 1 - 4 years acute seizure ?
5 mg.
476
What is the recommended dose for midazolam for children aged 5 - 9 years acute seizure ?
7.5 mg.
477
What is the recommended dose for midazolam for children aged 10 - 17 years acute seizure ?
10 mg.
478
What is the recommended dose for midazolam for adults acute seizures ?
10 mg (unlicensed).
479
480
What is the recommended adrenaline dose for infants under 6 months?
100 - 150 micrograms (0.1 - 0.15 ml 1 in 1,000) ## Footnote Doses are critical for effective anaphylaxis management.
481
What is the recommended adrenaline dose for children aged 6 months to 6 years?
150 micrograms (0.15 ml 1 in 1,000) ## Footnote Accurate dosing is essential for safety and efficacy.
482
What is the recommended adrenaline dose for children aged 6-12 years?
300 micrograms (0.3 ml 1 in 1,000) ## Footnote Dosing varies with age and weight.
483
What is the recommended adrenaline dose for adults and children over 12 years?
500 micrograms (0.5 ml 1 in 1,000) ## Footnote Adult dosing reflects greater body mass and potential severity.
484
How often can adrenaline be repeated in an anaphylaxis case?
Every 5 minutes if necessary ## Footnote Timely administration can be life-saving.
485
What is the best site for IM injection of adrenaline?
Anterolateral aspect of the middle third of the thigh ## Footnote Proper injection technique is crucial for absorption.
486
What defines refractory anaphylaxis?
Respiratory and/or cardiovascular problems persist despite 2 doses of IM adrenaline ## Footnote Indicates a severe, ongoing reaction requiring further intervention.
487
What should be given for shock in refractory anaphylaxis?
IV fluids ## Footnote Fluid resuscitation is important for stabilizing the patient.
488
What should be sought in cases of refractory anaphylaxis?
Expert help for consideration of an IV adrenaline infusion ## Footnote Advanced care may be necessary for severe cases.
489
What type of antihistamines may be given after initial stabilization?
Non-sedating oral antihistamines ## Footnote Preferable to chlorphenamine, especially for skin symptoms.
490
What is a potential challenge in diagnosing anaphylaxis?
Establishing whether a patient had a true episode of anaphylaxis ## Footnote Diagnosis can be complicated and may require serum tryptase levels.
491
How long can serum tryptase levels remain elevated after an acute episode of anaphylaxis?
Up to 12 hours ## Footnote Useful for confirming anaphylaxis diagnosis.
492
What should all patients with a new diagnosis of anaphylaxis be referred to?
A specialist allergy clinic ## Footnote Ongoing management and education are essential.
493
What interim measure should be given before a specialist allergy assessment?
An adrenaline injector ## Footnote Important for patient safety until further evaluation.
494
How many adrenaline auto-injectors should patients be prescribed?
2 adrenaline auto-injectors ## Footnote Ensures availability in case of multiple reactions.
495
What training should be provided to patients prescribed adrenaline auto-injectors?
Training on how to use the injector ## Footnote Proper use is critical for effectiveness.
496
What is the risk of biphasic reactions in patients with anaphylaxis?
Can occur in up to 20% of patients ## Footnote Monitoring post-discharge is important.
497
What is required for fast-track discharge after anaphylaxis?
Good response to a single dose of adrenaline, complete resolution of symptoms, given an adrenaline auto-injector, adequate supervision ## Footnote Fast-tracking is based on clinical stability.
498
What is the minimum observation time after symptom resolution for patients needing 2 doses of IM adrenaline?
6 hours ## Footnote Extended observation is critical for safety.
499
What conditions require a minimum of 12 hours observation after symptom resolution?
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 ## Footnote These factors increase risk for complications.
500

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