Friday 1st October Flashcards

1
Q

What is claudication? [1]

A

Pain in your thigh, calf or buttock when you walk

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2
Q

Key differential in patient presenting with claudication [1]

A

Spinal stenosis

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3
Q

Differentiate between spinal stenosis and peripheral arterial disease [4]

A

Pain improving on sitting down or crouches down
Weakness of the leg
Lack of smoking history
Lack of cardiovascular history

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4
Q

What is the most common presenting Sx in AS? [1]

A

Back pain

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5
Q

What is lumbar spinal stenosis? [1]

A

Lumbar spinal stenosis is a condition in which the central canal is narrowed by tumour, disk prolapse or other similar degenerative changes.

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6
Q

How to differentiate true claudication [1]

A

Sitting is better than standing and patients may find it easier to walk uphill rather than downhill. T

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7
Q

What is the most common underlying cause for spinal stenosis? [1]

A

Degenerative disease is the commonest underlying cause.

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8
Q

Best way of Dx spinal stenosis [1]

A

MRI scanning is the best modality for demonstrating the canal narrowing.

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9
Q

What is the Tx for spinal stenosis? [1]

A

Laminectomy

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10
Q

When is the postmenopausal period? [1]

A

This woman has entered the postmenopausal period as she has not had a period for 12 months

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11
Q

Does a 47 y/o F with amenorrhoea for 12m require contraception and why? [2]

A

‘Women using non-hormonal methods of contraception can be advised to stop contraception after 1 year of amenorrhoea if aged over 50 years, 2 years if the woman is aged under 50 years.’

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12
Q

Best contraceptive option for a women with PMH of breast cancer [1]

A

A copper coil is the best option for this woman because of her past history of breast cancer

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13
Q

Which contraceptives are UKMEC1 for women over 40? [2]

A

All methods are UKMEC1 except for the combined oral contraceptive pill (UKMEC2 for women >= 40 years) and Depo-Provera (UKMEC2 for women > 45 years)

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14
Q

Why might a COPD be useful for women in peripmenopuasal period? [2]

A

COCP use in the perimenopausal period may help to maintain bone mineral density
COCP use may help reduce menopausal symptoms

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15
Q

Dose altering of COCP in women over 40? [1]

A

a pill containing < 30 µg ethinylestradiol may be more suitable for women > 40 years

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16
Q

What should women be warned about when taking Depot Provera over 40? [2]

A

women should be advised there may be a delay in the return of fertility of up to 1 year for women > 40 years
use is associated with a small loss in bone mineral density which is usually recovered after discontinuation

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17
Q

Can COPD be continued over the age of 50? [1]

A

No, switch to non-hormonal or progestogen-only method

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18
Q

Can implant/POP/IUS be continued past the age of 50? [3]

A

Continue

If amenorrhoeic check FSH and stop after 1 year if FSH >= 30u/l or stop at 55 years

If not amenorrhoeic consider investigating abnormal bleeding pattern

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19
Q

Can HRT be relied upon for contraception? [1]

A

As we know hormone replacement therapy (HRT) cannot be relied upon for contraception so a separate method of contraception is needed

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20
Q

What should mothers be offered if they have a PMH of a baby with GBS? [1]

A

Prescribe intrapartum IV benzylpenicillin

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21
Q

Why should benzylpenicillin not be given straight away to child? [1]

A

Administer intravenous benzylpenicillin to the child at birth is incorrect. Antibiotics should only be administered to the child if they present signs and symptoms of neonatal sepsis.

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22
Q

What is the most common cause of early-onset severe infection int he neonatal period? [1]

A

GBS

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23
Q

How many mothers are carriers of GBS? [1]

A

It is thought around 20-40% of mothers have GBS present in their bowel flora and may therefore be thought of as ‘carriers’ of GBS

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24
Q

RFs for GBS [4]

A

prematurity
prolonged rupture of the membranes
previous sibling GBS infection
maternal pyrexia e.g. secondary to chorioamnionitis

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25
What is the risk of GBS carriage in new pregnancy if they've already had it previous one? [1]
women who've had GBS detected in a previous pregnancy should be informed that their risk of maternal GBS carriage in this pregnancy is 50%
26
When should women have swabs for GBS? [1]
if women are to have swabs for GBS this should be offered at 35-37 weeks or 3-5 weeks prior to the anticipated delivery date
27
when should women be given IAP? [1]
women with a pyrexia during labour (>38ºC) should also be given IAP
28
Positive p24 and antibody test for HIV, what should happen? [2]
- started on anti-retroviral treatment today | - repeat HIV p24 and antibody in 12w time
29
When can post-exposure prophylaxis be commenced? [1]
Can only be started 72 hours after possible exposure [i.e. recent high risk sex]
30
How common is HIV seroconversion symptomatic in HIV patients? [1]
60-80%
31
Typical presentation of HIV seroconversion [1]
Glandular type fever illness
32
When does HIV seroconversion typically occur? [1]
3-12w after infection
33
Features of HIV seroconversion [3]
``` sore throat lymphadenopathy malaise, myalgia, arthralgia diarrhoea maculopapular rash mouth ulcers rarely meningoencephalitis ```
34
When do HIV antibodies develop? [1]
may not be present in early infection, but most people develop antibodies to HIV at 4-6 weeks but 99% do by 3 months
35
When does p24 antigen become testable? [2]
a viral core protein that appears early in the blood as the viral RNA levels rise usually positive from about 1 week to 3 - 4 weeks after infection with HIV
36
When should a HIV test be offered for possible exposure? [1]
testing for HIV in asymptomatic patients should be done at 4 weeks after possible exposure
37
What is the standard for HOV diagnosis and screening? [2]
combination tests (HIV p24 antigen and HIV antibody) are now standard for the diagnosis and screening of HIV
38
Most common CXR finding in PE? [1]
normal CXR
39
How common are tachypnea, crackles, tachycardia, fever in PE? [4]
The relative frequency of common clinical signs is shown below: Tachypnea (respiratory rate >20/min) - 96% Crackles - 58% Tachycardia (heart rate >100/min) - 44% Fever (temperature >37.8°C) - 43%
40
What is recommended as initial lung-imaging modality for non-massive PE? [1]
CTPA scan
41
Advantages of CTPA over V/Q scan [3]
Advantages compared to V/Q scans include speed, easier to perform out-of-hours, a reduced need for further imaging and the possibility of providing an alternative diagnosis if PE is excluded
42
If CTPA negative, are further tests required?
No, also no need Ix
43
When is V/Q scanning appropriate? [4]
V/Q scanning may be used initially if appropriate facilities exist, the chest x-ray is normal, and there is no significant symptomatic concurrent cardiopulmonary disease. V/Q scanning is also the investigation of choice if there is renal impairment (doesn't require the use of contrast unlike CTPA) Think could also be CI in pregnancy?
44
Sensitivity and specificity of D-dimers [1]
95-98% | Poor specificity
45
ECG changes in PE [3]
- the classic ECG changes seen in PE are a large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III - 'S1Q3T3'. - right bundle branch block and right axis deviation are also associated with PE - sinus tachycardia may also be seen
46
How common is S1Q3T3? [1]
20% only of PE patients
47
Why is CXR ordered in PE? [1]
to r/o other causes
48
What might be found CXR in PE? [2]
Wedge-shaped opacification | Typically normal though
49
Sensitivity and specificity of V/Q scan [2]
sensitivity of around 75% and specificity of 97%
50
What type of brain injury is a lucid interval associated with? [1]
EDH
51
Types of primary brain injury [2]
Focal [contusion/haematoma] or diffuse [diffuse axonal injury]
52
How can diffuse axonal injuries occur? [1]
diffuse axonal injury occurs as a result of mechanical shearing following deceleration, causing disruption and tearing of axons
53
Where do contusions occur? [1]
contusions may occur adjacent to (coup) or contralateral (contre-coup) to the side of impact
54
When do secondary brain injuries occur? [4]
secondary brain injury occurs when cerebral oedema, ischaemia, infection, tonsillar or tentorial herniation exacerbates the original injury
55
What happens to the brain in secondary brain injuries? [2]
The normal cerebral auto regulatory processes are disrupted following trauma rendering the brain more susceptible to blood flow changes and hypoxia
56
What is Cushing reflex and when does it occur? [3]
the Cushings reflex (hypertension and bradycardia) often occurs late and is usually a pre terminal event
57
Where do EDH typically occur? [2]
The majority of epidural haematomas occur in the temporal region where skull fractures cause a rupture of the middle meningeal artery.
58
Features of EDH [2]
Raised ICP | Some patients have lucid interval
59
When do EDH typically occur? [1]
Often results from acceleration-deceleration trauma or a blow to the side of the head
60
Where do SDH typically occur? [1]
Most commonly occur around the frontal and parietal lobes.
61
RFs for SDH [3]
Risk factors include old age, alcoholism and anticoagulation.
62
Compare SDH to EDH [2]
Slower onset of symptoms than a epidural haematoma. There may be fluctuating confusion/consciousness
63
Classically, how does a subarachnoid haemorrhage present? [1]
Classically causes a sudden occipital headache.
64
When does SaH commonly occur? [2]
Usually occurs spontaneously in the context of a ruptured cerebral aneurysm but may be seen in association with other injuries when a patient has sustained a traumatic brain injury
65
What is a intracerebral haematoma? [1]
An intracerebral (or intraparenchymal) haemorrhage is a collection of blood within the substance of the brain
66
Causes/RF of ICH [5]
Causes / risk factors include: hypertension, vascular lesion (e.g. aneurysm or arteriovenous malformation), cerebral amyloid angiopathy, trauma, brain tumour or infarct (particularly in stroke patients undergoing thrombolysis).
67
Why is it crucial to obtain a CT in head in all stroke patients prior to thrombolysis? [2]
Patients will present similarly to an ischaemic stroke in ICH Or will present with decreased LOC
68
Blood profile of a patient with anaemia of chronic disease [4]
A normocytic anaemia with low serum iron, low TIBC but raised ferritin in a patient with a chronic illness is typical of anaemia of chronic disease
69
Three distinct pathological processes in iron profile of anaemia of chronic disease [3]
reduced iron release from marrow, inadequate secretion of EPO for erythropoiesis and reduced red cell survival
70
Why is ferritin raised in chronic inflammation? [1]
Ferritin is an acute phase reactant and therefore raised in states of chronic inflammation, as is likely to be the case in this patient.
71
Why are platelets raised in chronic anaemia? [1]
The platelets are raised due to a reactive thrombocytosis in the presence of inflammation.
72
Blood profile of iron defieicny anaemia [3]
Iron deficiency anaemia causes a microcytic anaemia, low ferritin and a raised TIBC
73
Hereditary haemochromatosis blood picture [3]
Hereditary haemochromatosis can cause a raised ferritin and low TIBC however iron levels are unlikely to be normal and ferritin would usually be much higher than in this case.
74
What does sidroblastic anaemias typically cause blood profile? [2]
Sideroblastic anaemia usually causes a microcytic anaemia with raised serum iron levels.
75
Causes of normocytic anaemias [5]
``` anaemia of chronic disease chronic kidney disease aplastic anaemia haemolytic anaemia acute blood loss ```
76
What should be offered to patients with intrahepatic cholestasis and why? [2]
Intrahepatic cholestasis of pregnancy increases the risk of stillbirth; therefore induction of labour is generally offered at 37-38 weeks gestation
77
how common is intrahepatic cholestasis in pregnancy? [1]
1% in the UK
78
Features of intrahepatic cholestasis of pregnancy [3]
pruritus - may be intense - typical worse palms, soles and abdomen clinically detectable jaundice occurs in around 20% of patients raised bilirubin is seen in > 90% of cases
79
Mx of cholestasis of pregnancy [3]
induction of labour at 37-38 weeks is common practice but may not be evidence based ursodeoxycholic acid - again widely used but evidence base not clear vitamin K supplementation
80
How common is recurrence of intrahepatic cholestasis of pregnancy? [1]
Recurrence of intrahepatic cholestasis of pregnancy is 45-90% in subsequent pregnancies.
81
Presentation of biliary colic vs cholecystitis [4]
The pain becomes worse after eating but she is generally well, afebrile and her abdomen is soft. In cholecystitis, you would expect evidence of infection (e.g. fever, tachycardia). You might also be able to palpate the gallbladder, and she may be Murphy's sign positive.
82
What is ERCP procedure used for? [1]
ERCP is a procedure that can be used to remove obstructing gallstones from the common bile duct or pancreatic duct, so has no role in simple biliary colic
83
Signs of an obstructing stone include what? [1]
Signs of an obstructing stone would include jaundice, of which there is no mention here
84
What is biliary colic caused by? [1]
Biliary colic is caused by gallstones passing through the biliary tree.
85
RFs for biliary colic [4]
it is traditional to refer to the '4 F's': Fat: obesity is thought to be a risk factor due to enhanced cholesterol synthesis and secretion Female: gallstones are 2-3 times more common in women. Oestrogen increases activity of HMG-CoA reductase Fertile: pregnancy is a risk factor Forty
86
Other notable RFs for biliary colic [4]
diabetes mellitus Crohn's disease rapid weight loss e.g. weight reduction surgery drugs: fibrates, combined oral contraceptive pill
87
Simple PP of biliary colic [3]
occur due to ↑ cholesterol, ↓ bile salts and biliary stasis | the pain occurs due to the gallbladder contracting against a stone lodged in the cystic duct
88
Features of biliary colic [3]
colicky right upper quadrant abdominal pain worse postprandially, worse after fatty foods the pain may radiate to the right shoulder/interscapular region nausea and vomiting are common
89
Ix for biliary colic [1]
ultrasound
90
Mx of biliary colic [1]
- elective laparoscopic cholecystectomy
91
How common is it to have gallstones in the common bile duct? [1]
Around 15% of patients are found to have gallstones in the common bile duct (choledocholithiasis) at the time of cholecystectomy, This can result in obstructive jaundice in some patients
92
Possible Cx other than biliary colic of a gallstone [5]
``` acute cholecystitis: the most common complication ascending cholangitis acute pancreatitis gallstone ileus gallbladder cancer ```
93
What is most likely to be observed in the synovial fluid taken from a patients knee with reactive arthritis? [2]
Sterile synovial fluid with a high WCC
94
24 y/o painful right knee, lethargy, feverish Sx, PMH includes chlaydia infection 2w previously. Dx? [1]
Septic arthritis
95
Define reactive arthritis [3]
The patient's presentation is suggestive of reactive arthritis, a HLA-B27 seronegative spondyloarthritis classically associated with oligoarthritis of the lower limbs following a gastrointestinal or urogenital infection 1-4 weeks previously
96
What type of WBCs will be seen in synovial fluid of patient with reactive arthritis? [1]
The pathological process is aseptic, does not involve salt crystal formation, but is likely to cause increased white blood cells in the fluid (mostly polymorphonuclear leukocytes).
97
When are negatively birefringent crystals seen in pts? [2]
commonly seen in calcium pyrophosphate deposition (pseudogout).
98
Positively birefringent crystals seen commonly when? [1]
Gout
99
What are smears done to test? [1]
Cervical cancer
100
What should happen if 2 consecutive inadequate samples taken cervical smear? [1]
Refer to colposcopy
101
Which system does the cervical cancer screening employ currently? [2]
The NHS has now moved to an HPV first system, i.e. a sample is tested for high-risk strains of human papillomavirus (hrHPV) first and cytological examination is only performed if this is positive.
102
If patient has negative hrHPV, what should you do? [5]
return to normal recall, unless the test of cure (TOC) pathway: individuals who have been treated for CIN1, CIN2, or CIN3 should be invited 6 months after treatment for a test of cure repeat cervical sample in the community the untreated CIN1 pathway follow-up for incompletely excised cervical glandular intraepithelial neoplasia (CGIN) / stratified mucin producing intraepithelial lesion (SMILE) or cervical cancer follow-up for borderline changes in endocervical cells
103
If hrHPV is positive and cytology is abnormal, what should be next line Mx? [1]
if the cytology is abnormal → colposcopy
104
If cytology is normal, but hrHPV is abnormal, what should be done? [1]
if the cytology is normal (i.e. hrHPV +ve but cytologically normal) the test is repeated at 12 months
105
If cervical sample is inadequate [2]
repeat the sample within 3 months | if two consecutive inadequate samples then → colposcopy
106
Inherited causes of thrombophilia [5]
Gain of function polymorphisms - factor V Leiden (activated protein C resistance): most common cause of thrombophilia - prothrombin gene mutation: second most common cause Deficiencies of naturally occurring anticoagulants - antithrombin III deficiency - protein C deficiency - protein S deficiency
107
Prevalence and RR of VTE in factor V Leiden [heterozygous]
prevalence 5%, relative risk of VTE is 4
108
Prevalence and RR of VTE in protein C deficiency
0.3% and RR is 10
109
Acquired causes of thrombophilia [2]
Antiphospholipid syndrome Drugs the combined oral contraceptive pill
110
What is Hodgkins lymphoma? [2]
Hodgkin's lymphoma is a malignant proliferation of lymphocytes characterised by the presence of the Reed-Sternberg cell
111
When is Hodgkin's lymphoma most common? [1]
It has a bimodal age distributions being most common in the third and seventh decades
112
What is the most common type of HL? [1]
nodular sclerosing
113
Features of nodular sclerosing HL [3]
More common in women. Associated with lacunar cells | Good prognosis
114
Which HL type has best prognosis, which has the worst prognosis? [2]
Lymphocyte predominant [5%] best prognosis, lymphocyte depleted [rare] worst prognosis
115
What is HSP? [2]
HSP is a IgA mediated small vessel vasculitis
116
When is HSP seen? [1]
Usually seen in children following an infection
117
Features of HSP [4]
palpable purpuric rash (with localized oedema) over buttocks and extensor surfaces of arms and legs abdominal pain polyarthritis features of IgA nephropathy may occur e.g. haematuria, renal failure
118
Tx for HSP [2]
analgesia for arthralgia treatment of nephropathy is generally supportive. There is inconsistent evidence for the use of steroids and immunosuppressants
119
Prognosis of HSP [2]
usually excellent, HSP is a self-limiting condition, especially in children without renal involvement around 1/3rd of patients have a relapse
120
Where is Legionnaire's disease typically contracted from? [1]
It typically colonizes water tanks and hence questions may hint at air-conditioning systems or foreign holidays.
121
Is Legionaires transmittable? [1]
No not person-to-person
122
Features of Legionella [8]
``` flu-like symptoms including fever (present in > 95% of patients) dry cough relative bradycardia confusion lymphopaenia hyponatraemia deranged liver function tests pleural effusion: seen in around 30% of patients ```
123
Are lymphocytes raised/depressed in Legionella? [1]
Depressed -> lymphopaenia not lymphocytosis
124
Dx of Legionella [1]
Urinary antigen
125
Tx of Legionella [1]
Tx with erythromycin/clarithromycin
126
Similarities between Legionella and Mcyoplasma pneumonia [5]
``` Atypical presentation Flu-like Sx Dry cough Deranged LFTs treat with macrolide [e.g. erhyromycin] ```
127
Which tool is used for postnatal depression? [2]
Edinburgh scale [or the PHQ-9]
128
GAD-7 questionnaire used for? [1]
anxiety
129
Bishop score [1]
informing the induction of labour
130
FAST and CAGE score [2]
alcoholism
131
What are the baby-blues? [4]
- seen i around 60-70% of women - typically seen 3-7d following birth and more common primips - mothers anxious/irritbale/tearful - reassurance and support needed
132
How common is PND? [1]
Typically 10% of mothers
133
When does PND start? [1]
Most within a month, typically peaking at around 3m
134
Sx of PND [1]
Similar to depression
135
Mx of PND [3]
CBT may be beneficial | Certain SSRIs such as sertraline/paroxetine if Sx severe
136
Are SSRIs harmful to the baby? [1]
Secreted breast milk, but not harmful
137
Features of puerperal psychosis [2]
Features include severe swings in mood (similar to bipolar disorder) and disordered perception (e.g. auditory hallucinations)
138
How common is puerperal psychosis, and when does onset occur? [2]
Affects approximately 0.2% of women | Onset usually within the first 2-3 weeks following birth
139
Mx of puerperal psychosis [1]
Admission to hospital is usually required
140
Risk of recurrence of puerperal psychosis [1]
There is around a 25-50% risk of recurrence following future pregnancies
141
What is glandular fever also known as? [1]
Infectious mononucleosis
142
What is infectious mononucleosis caused by in 90% of cases? [1]
EBV [also know as human herpesvirus 4]
143
Other causes of glandular fever [2]
Cytomegalovirus
144
Population most common in IM [1]
Adolescents and young adults
145
What is the classic triad seen in 98% of IM patients? [3]
Sore throat Lymphadenopathy Pyrexia
146
Difference in lymphadenopathy of IM compared to tonsillitis [1]
may be present in the anterior and posterior triangles of the neck, in contrast to tonsillitis which typically only results in the upper anterior cervical chain being enlarged
147
Other features of IM [3]
malaise, anorexia, headache palatal petechiae splenomegaly - occurs in around 50% of patients and may rarely predispose to splenic rupture hepatitis, transient rise in ALT lymphocytosis: presence of 50% lymphocytes with at least 10% atypical lymphocytes haemolytic anaemia secondary to cold agglutins (IgM) a maculopapular, pruritic rash develops in around 99% of patients who take ampicillin/amoxicillin whilst they have infectious mononucleosis
148
What happens to patients 99% of patients treated with ampicillin/amoxicillin whilst they have IM? [1]
a maculopapular, pruritic rash develops in around 99% of patients who take ampicillin/amoxicillin whilst they have infectious mononucleosis
149
How to Dx IM? [1]
heterophil antibody test (Monospot test) - NICE guidelines suggest FBC and Monospot in the 2nd week of the illness to confirm a diagnosis of glandular fever.
150
Mx of glandular fever [3]
rest during the early stages, drink plenty of fluid, avoid alcohol simple analgesia for any aches or pains consensus guidance in the UK is to avoid playing contact sports for 8 weeks after having glandular fever to reduce the risk of splenic rupture
151
How should people exposed to a patient with confirmed bacterial meningitis be Tx? [1]
People who have been exposed to a patient with confirmed bacterial meningitis should be given prophylactic antibiotics if they have close contact within the seven days before onset
152
In a young student, what is the common causative organism for bacterial meningitis? [2]
Neisseria meningitidis and Streptococcus pneumoniae
153
Ix for meningitis [8]
``` Investigations suggested by NICE full blood count CRP coagulation screen blood culture whole-blood PCR blood glucose blood gas ``` Lumbar puncture
154
When should you not do an LP in meningitis? [1]
Signed of raised ICP
155
If patient is waiting and is meningococcal disease is suspected, what should be given? [1]
intramuscular benzylpenicillin may be given, as long as this doesn't delay transit to hospital.
156
Initial empirical therapy for patients aged 3 to 50 y/ [1]o
IV cefotaxime [or ceftriaxone]
157
Rx for patient with confirmed IV meningococcal meningitis [1]
Intravenous benzylpenicillin or cefotaxime (or ceftriaxone)
158
What should also be given alongside abx for meningitis? When should this be withheld? [5]
``` Intravenous dexamethasone should also be given to reduce the risk of neurological sequelae, but the BNF advise to withhold if: septic shock meningococcal septicaemia immunocompromised meningitis following surgery ```
159
Which drug to give if patient has hypersensitivity to penicillin or cephalosporins? [1]
Chloramphenicol
160
Close contact how many days before onset meningitis prophylaxis? [1]
7 days
161
Which drug should be given close contact meningitis 7 days previously? [2]
oral ciprofloxacin or rifampicin or may be used. The Health Protection Agency (HPA) guidelines now state that whilst either may be used ciprofloxacin is the drug of choice as it is widely available and only requires one dose
162
Two main ways of AAA presenting [2]
The presentation of a tuptured abdominal aortic aneurysm (AAA) may be catastrophic (e.g. sudden collapse) or sub-acute (persistent severe central abdominal pain with developing shock).
163
Features of an AAA
central abdominal pain radiating to the back pulsatile mass in the abdomen patients may be shocked (hypotension, tachycardic)
164
What is the single most important step definitive Mx of patient's condition with AAA? [1]
Seek immediate vascular review
165
how is an AAA typically diagnosed? [1]
The diagnosis is clinical, these patients are not stable enough for a CT scan etc to confirm the diagnosis.
166
What would inferior STEMI look like on an ECG? [1]
An inferior STEMI would cause ST elevation in leads II, III and aVF
167
What would lateral STEMI look like on an ECG? [1]
ST elevation in leads I, aVL and V5-V6
168
What would NSTEMI look like on an ECG? [3]
In an NSTEMI, there may be signs of ischaemia on ECG, for example ST depression, T-wave changes or transient ST elevation, or it may be normal.
169
What would LVH show on an ECG? [2]
sum of S wave in V1 and R wave in V5 or V6 exceeds 40 mm
170
What would RVH show on an ECG? [4]
RVH is diagnosed on ECG in the presence of a R/S ratio of greater than 1 in lead V1 in the absence of other causes, or if the R wave in lead V1 is greater than 7 millimeters tall. The strain pattern occurs when the right ventricular wall is quite thick, and the pressure is high, as well. Strain causes ST segment depression and asymmetric T wave inversions in leads V1 to V3.
171
What is the commonest skin disorder in pregnancy? [1]
Atopic eruption in pregnancy
172
Features of atopic eruption pregnancy [2]
it typically presents as an eczematous, itchy red rash. | no specific treatment is needed
173
Features of polymorphic eruption of pregnancy [3]
pruritic condition associated with last trimester lesions often first appear in abdominal striae management depends on severity: emollients, mild potency topical steroids and oral steroids may be used
174
Features of pemphigoid gestations [4]
pruritic blistering lesions often develop in peri-umbilical region, later spreading to the trunk, back, buttocks and arms usually presents 2nd or 3rd trimester and is rarely seen in the first pregnancy oral corticosteroids are usually required
175
What type of drug is lidocaine? [1]
Amide
176
How does it work and does this mean it's used for? [2]
Local anaesthetic and less commonly anti arrhythmic [affects Na channels in the axon]
177
How can lidocaine toxicity occur? [2]
Toxicity: due to IV or excess administration. Increased risk if liver dysfunction or low protein states. Note acidosis causes lidocaine to detach from protein binding
178
How can local anaesthetic toxicity be treated? [1]
Local anesthetic toxicity can be treated with IV 20% lipid emulsion
179
Concentration of cocaine used clinically [1]
It is supplied for clinical use in concentrations of 4 and 10%
180
how is cocaine applied? [1]
It may be applied topically to the nasal mucosa
181
How does cocaine act? [1]
It has a rapid onset of action and has the additional advantage of causing marked vasoconstriction.
182
Systemic effects of cocaine [1]
Its systemic effects also include cardiac arrhythmias and tachycardia.
183
When is it used medicine? [1]
Apart from its limited use in ENT surgery it is otherwise used rarely in mainstream surgical practice.
184
How does bupivacaine work? [2]
Bupivacaine binds to the intracellular portion of sodium channels and blocks sodium influx into nerve cells, which prevents depolarization.
185
Advantage of bupivacaine over lignocaine [1]
It has a much longer duration of action than lignocaine and this is of use in that it may be used for topical wound infiltration at the conclusion of surgical procedures with long duration analgesic effect.
186
When is Bupivacaine contra-indicated and what is used as a replacement? [2]
It is cardiotoxic and is therefore contra indicated in regional blockage in case the tourniquet fails. Levobupivicaine (Chirocaine) is less cardiotoxic and causes less vasodilation.
187
When is Prilocaine used? [1]
Similar mechanism of action to other local anaesthetic agents. However, it is far less cardiotoxic and is therefore the agent of choice for intravenous regional anaesthesia e.g. Biers Block.
188
Why is adrenaline sometimes added to local anaesthetics? [2]
Adrenaline may be added to local anaesthetic drugs. It prolongs the duration of action at the site of injection and permits usage of higher doses (see above)
189
When is adrenaline CI for use with local anaesthetics? [1]
It is contra indicated in patients taking MAOI's or tricyclic antidepressants.
190
What type of incontinence is caused by bladder still palpable after urination? [1]
think retention with urinary overflow
191
Most common cause of urinary overflow incontinence [1]
Prostate problems
192
Causes of urinary overflow incontinence in a women [3]
Other causes can include nerve damage causing a neurogenic bladder such as complication of diabetics, chronic alcoholics or surgery to the pelvic area.
193
Sx of overactive balder [1]
An overactive bladder syndrome is a form of urge incontinence caused by an overactive bladder, it too would be associated with incontinence, polyuria and nocturia.
194
What is mixed urinary incontinence? [2]
urge and stress incontience combined
195
RFs for urinary incontinence [5]
``` advancing age previous pregnancy and childbirth high body mass index hysterectomy family history ```
196
OAB definition [1]
overactive bladder (OAB)/urge incontinence: due to detrusor overactivity
197
Stress classification [1]
leaking small amounts when coughing or laughin
198
overflow incontinence [1]
overflow incontinence: due to bladder outlet obstruction, e.g. due to prostate enlargement
199
Initial Ix for incontinence [4]
bladder diaries should be completed for a minimum of 3 days vaginal examination to exclude pelvic organ prolapse and ability to initiate voluntary contraction of pelvic floor muscles ('Kegel' exercises) urine dipstick and culture urodynamic studies
200
Mx of urge incontinence [3]
bladder retraining bladder stabilising drugs mirabegron
201
How long should bladder retraining take? [1]
lasts for a minimum of 6 weeks, the idea is to gradually increase the intervals between voiding)
202
Drugs to give for bladder stabilising effects in urge incontinence [3]
antimuscarinics are first-line. NICE recommend oxybutynin (immediate release), tolterodine (immediate release) or darifenacin (once daily preparation). Immediate release oxybutynin should, however, be avoided in 'frail older women'
203
Which drug should be given to frail older women with incontinence for bladder stabilising? [1]
mirabegron (a beta-3 agonist) may be useful if there is concern about anticholinergic side-effects in frail elderly patients
204
Stress incontinence Mx [3]
- Pelvic floor muscle training - Surgical procedures [e.g. retropubic mid-urethral tap procedures] - Duloxetine if declined surgical procedures
205
Pelvic floor muscle training how is it done? [1]
NICE recommend at least 8 contractions performed 3 times per day for a minimum of 3 months
206
How does duloxetine work for women with stress incontinence? [2]
a combined noradrenaline and serotonin reuptake inhibitor mechanism of action: increased synaptic concentration of noradrenaline and serotonin within the pudendal nerve → increased stimulation of urethral striated muscles within the sphincter → enhanced contraction
207
How does presbycusis present? [1]
Presbycusis presents with bilateral high-frequency hearing loss
208
What is presbycusis? [1]
Age related sensorineural deafness, initially affecting high-frequency tones. Particularly in noisy envirnoments.
209
Why type of conduction is greater in sensoryneural hearing loss? [1]
Air conduction is superior to bone conduction
210
Epidemiology of presbycusis [3]
In the USA, it is estimated that 25-30% of 65-74 year-olds have impaired hearing. For those over 75 years, the incidence is 40-50% The age of presentation varies, however, prevalence increases with age Males are at slightly higher risk of developing presbycusis compared to females (55%:45%)
211
Causes of presbycusis [3]
The precise cause is unknown however is likely multifactorial Arteriosclerosis: May cause diminished perfusion and oxygenation of the cochlea, resulting in damage to inner ear structures Diabetes: Acceleration of arteriosclerosis Accumulated exposure to noise Drug exposure (Salicylates, chemotherapy agents etc.) Stress Genetic: Certain individuals may be programmed for the early ageing of the auditory system
212
Presentation of presbycusis [3]
Speech becoming difficult to understand Need for increased volume on the television or radio Difficulty using the telephone Loss of directionality of sound Worsening of symptoms in noisy environments Hyperacusis: Heightened sensitivity to certain frequencies of sound (Less common) Tinnitus (Uncommon)
213
Ix can be done for presbycusis, what will they show? [8]
Otoscopy: Normal, to rule out otosclerosis, cholesteatoma and conductive hearing loss (Foreign body, impacted wax etc.) Tympanometry: Normal middle ear function with hearing loss (Type A) Audiometry: Bilateral sensorineural pattern hearing loss Blood tests including inflammatory markers and specific antibodies: Normal
214
Audiometry in presbycusis [1]
Bilateral sensorineural pattern hearing loss
215
Mx of acute pancreatitis? [1]
Fluids and analgesia [Abx should not be routinely Rx]
216
What is flank discolouration a sign of? [1]
The flank discolouration is consistent with Grey-Turner's sign, which although rare in practice, is a common finding in exam questions and it is classically associated with acute pancreatitis
217
What fluids should be offered for acute pancreatitis? [3]
fluid resuscitation - aggressive early hydration with crystalloids. In severe cases 3-6 litres of third space fluid loss may occur - aim for a urine output of > 0.5mls/kg/hr - may also help relieve pain by reducing lactic acidosis
218
Which analgesia commonly given acute pancreatitis? [1]
pain may be severe so this is a key priority of care | intravenous opioids are normally required to adequately control the pain
219
How should patients have their nutrition? [3]
- patients should not routinely be made 'nil-by-mouth' unless there is a clear reason e.g. the patient is vomiting - enteral nutrition should be offered to anyone with moderately severe or severe acute pancreatitis within 72 hours of presentation - parental nutrition should only be used if enteral nurition has failed or is contraindicated
220
What is the role of antibiotics in acute pancreatitis? [2]
NICE state the following: 'Do not offer prophylactic antimicrobials to people with acute pancreatitis' potential indications include infected pancreatic necrosis
221
What is the role of surgery in acute pancreatitis? [4]
Patients with acute pancreatitis due to gallstones should undergo early cholecystectomy Patients with obstructed biliary system due to stones should undergo early ERCP Patients who fail to settle with necrosis and have worsening organ dysfunction may require debridement, fine needle aspiration is still used by some Patients with infected necrosis should undergo either radiological drainage or surgical necrosectomy. The choice of procedure depends upon local expertise
222
What is erythema ab igne? [1]
Erythema ab igne is a skin disorder caused by over exposure to infrared radiation.
223
Characteristic features of erythema ab igne [4]
Characteristic features include reticulated, erythematous patches with hyperpigmentation and telangiectasia.
224
Typical history of erythema ab ignore [1]
A typical history would be an elderly women who always sits next to an open fire.
225
Why is it important to Tx erythema ab igne? [1]
Squamous cell skin cancer may develop
226
When is a nuchal translucency performed? [1]
11-13w
227
Causes of increased nuchal transluscency [3]
Down's syndrome congenital heart defects abdominal wall defects
228
Causes of hyperchogenic bowel on a NL [3]
cystic fibrosis Down's syndrome cytomegalovirus infection
229
What can prolonged, untreated secondary hyperparathyroidism lead to? [1]
Tertiary hyperparathyroidism
230
Signs of hypercalcamia [5]
Worsening fatigue, thirst, anorexia, general aches and pains
231
Hormone profile or primary vs secondary vs tertiary hyperparathyroidism [3]
Primary hyperparathyroidism - PTH (Elevated) - Ca2+ (Elevated) - Phosphate (Low) - Urine calcium : creatinine clearance ratio > 0.01 Secondary - PTH (Elevated) - Ca2+ (Low or normal) - Phosphate (Elevated) - Vitamin D levels (Low) Tertiary hyperparathyroidism - Ca2+ (Normal or high) - PTH (Elevated) - Phosphate levels (Decreased or Normal) - Vitamin D (Normal or decreased) - Alkaline phosphatase (Elevated)
232
Clinical features of primary vs secondary vs tertiary hyperparathyroidism [3]
Primary - May be asymptomatic if mild - Recurrent abdominal pain (pancreatitis, renal colic) - Changes to emotional or cognitive state Secondary - May have few symptoms - Eventually may develop bone disease, osteitis fibrosa cystica and soft tissue calcifications Tertiary - Metastatic calcification - Bone pain and / or fracture - Nephrolithiasis - Pancreatitis
233
Cause of primary vs secondary vs tertiary hyperparathyroidism [3]
Primary - Most cases due to solitary adenoma (80%), multifocal disease occurs in 10-15% and parathyroid carcinoma in 1% or less Secondary - Parathyroid gland hyperplasia occurs as a result of low calcium, almost always in a setting of chronic renal failure Tertiary - Occurs as a result of ongoing hyperplasia of the parathyroid glands after correction of underlying renal disorder, hyperplasia of all 4 glands is usually the cause
234
Ddx of hyperparathyoidism [1]
It is important to consider the rare but relatively benign condition of benign familial hypocalciuric hypercalcaemia, caused by an autosomal dominant genetic disorder. Diagnosis is usually made by genetic testing and concordant biochemistry (urine calcium : creatinine clearance ratio <0.01-distinguished from primary hyperparathyroidism).
235
Tx for primary hyperparathyroidism [3]
Indications for surgery: Elevated serum Calcium > 1mg/dL above normal Hypercalciuria > 400mg/day Creatinine clearance < 30% compared with normal Episode of life threatening hypercalcaemia Nephrolithiasis Age < 50 years Neuromuscular symptoms Reduction in bone mineral density of the femoral neck, lumbar spine, or distal radius of more than 2.5 standard deviations below peak bone mass (T score lower than -2.5)
236
Mx of secondary hyperparathyroidism [4]
Usually managed with medical therapy. Indications for surgery in secondary (renal) hyperparathyroidism: Bone pain Persistent pruritus Soft tissue calcifications
237
Mx of tertiary hyperparathyroidism [2]
Allow 12 months to elapse following transplant as many cases will resolve The presence of an autonomously functioning parathyroid gland may require surgery. If the culprit gland can be identified then it should be excised. Otherwise total parathyroidectomy and re-implantation of part of the gland may be required.
238
Patients Dx with pneumonia who have COPD should be given what? [1]
Patients diagnosed with pneumonia who have COPD should be given corticosteroids even if no evidence of the COPD being exacerbated e.g. prednisolone 30mg
239
Primary vs secondary care setting for looking after patient with pneumonia
Primary - CRB65 Secondary - CURB65
240
Criteria of CURB65
``` Confusion [AMM over 8/10] Urea [over 7mmol/l] RR [equal or over 30/m] Blood pressure [systolic equal or over 90mmHg and/or diastolic over 60mmHg] Age [65 or over] ```
241
Recommendation for CURB65 score
``` 0-1 = consider home-based care 2+ = consider hospital-based care 3+ = consider intensive care ```
242
Ix for patients with pneumonia who have COPD
chest x-ray in intermediate or high-risk patients NICE recommend blood and sputum cultures, pneumococcal and legionella urinary antigen tests CRP monitoring is recommend for admitted patients to help determine response to treatment
243
First-line Mx of low-severity CAP [3]
amoxicillin is first-line if penicillin allergic then use a macrolide or tetracycline NICE now recommend a 5 day course of antibiotics for patients with low severity community acquired pneumonia
244
Mx of moderate to high-severity CAP [3]
if penicillin allergic then use a macrolide or tetracycline | NICE now recommend a 5 day course of antibiotics for patients with low severity community acquired pneumonia
245
How does critical limb ischaemia typically present? [2]
Critical limb ischaemia presents as pain at rest for greater than 2 weeks, often at night, not helped by analgesia
246
What is critical limb ischaemia caused by? [1]
Critical limb ischaemia is caused due to reduced amounts of oxygenated blood reaching the tissues of the lower limbs, most commonly secondary to atherosclerosis
247
What is CLI initially? [1]
Initially, peripheral arterial disease presents as intermittent claudication. However, as the disease progresses, pain becomes present at rest.
248
How to differentiate between CLI and acute limb ischaemia? [1]
Unlike acute limb ischaemia, this patient's limbs still have palpable peripheral pulses (6Ps of acute limb ischaemia: pain, perishingly cold, pallor, paraesthesia, paralysis, pulseless).
249
Why is acute limb ischaemia an emergency? [1]
However, if not treated promptly, this patient may develop acute limb ischaemia which is a limb-threatening emergency.
250
Features of CLI [3]
However, if not treated promptly, this patient may develop acute limb ischaemia which is a limb-threatening emergency.
251
What do patients often report with CLI? [1]
hanging their legs out of bed at night
252
What is an ABPI for CLI? [1]
Over 0.5
253
What is pernicious anaemia? [2]
Pernicious anaemia is an autoimmune disorder affecting the gastric mucosa that results in vitamin B12 deficiency.
254
Causes of B12 deficiency [3]
Whilst pernicious anaemia is the most common cause of vitamin B12 deficiency, it's not the only cause. Other causes include atrophic gastritis (e.g. secondary to H. pylori infection), gastrectomy, malnutrition (e.g. alcoholism).
255
PP of pernicious anaemia
antibodies to intrinsic factor +/- gastric parietal cells - intrinsic factor antibodies → bind to intrinsic factor blocking the vitamin B12 binding site - gastric parietal cell antibodies → reduced acid production and atrophic gastritis. Reduced intrinsic factor production → reduced vitamin B12 absorption
256
Why is vitamin B12 important in bodies? [2]
vitamin B12 is important in both the production of blood cells and the myelination of nerves → megaloblastic anaemia and neuropathy
257
RFs for pernicious anaemia [3]
more common in females (F:M = 1.6:1) and typically develops in middle to old age associated with other autoimmune disorders: thyroid disease, type 1 diabetes mellitus, Addison's, rheumatoid and vitiligo more common if blood group A
258
Features of pernicious anaemia [3]
Anaemia - lethargy - pallor - dyspnoea Neurological - peripheral neuropathy - subacute combined degeneration of the spinal cord - neuropsychiatric features like memory loss and depression Other - mild jaundice -> combined with pallor -> 'lemon tinge' - glossitis => sore tongue
259
Ix for pernicious anaemia [3]
FBC - microcytic anaemia: macrocytosis may be absent in 30% patients - hyperhsegmented polymorphs on blood film - low WCC and platelets my also be seen Vitamin and folate levels - vitamin B12 level of 200nh/L generally considered normal Antibodies - anti-intrinsic factor antibodies: sensitivity is only 50% but highly specific for pernicious anaemia [95-100%] - anti gastric parietal cell antibodies in 90% but low specificity often not useful
260
Mx of B12 deficiency [2]
vitamin B12 replacement - usually given intramuscularly - no neurological features: 3 injections per week for 2 weeks followed by 3 monthly treatment of vitamin B12 injections - more frequent doses are given for patients with neurological features - there is some evidence that oral vitamin B12 may be effective for providing maintenance levels of vitamin B12 but it is not yet common practice - folic acid supplementation may also be required
261
How vitamin B12 is replaced in pernicious anaemia with no neurological features? [2]
3 injections per week for 2w, followed by 3 monthly Tx of vitamin B12 injections
262
Cx other than haematological and neurological features [1]
increased risk of gastric cancer
263
When to consider gastric lavage for tricyclic OD? What else can be given? [2]
Consider gastric OD only within 1 hour of potentially fatal OD 50g of charcoal if within 1h ingestion
264
What to give to treat tricyclic OD? [1]
IV sodium bicarbonate [50ml of 8.4%]
265
When to give sodium bicarbonate in OD? [4]
pH <7.1 QRS >160 ms Arrhythmias Hypotension
266
When is IV adenosine given? [1]
Adenosine is used in the management of supraventricular tachycardia.
267
Which tricyclics are particularly dangerous? [1]
Overdose of tricyclic antidepressants is a common presentation to emergency departments. Amitriptyline and dosulepin (dothiepin) are particularly dangerous in overdose.
268
What are early features related to tricyclic OD? [2]
Early features relate to anticholinergic properties: dry mouth, dilated pupils, agitation, sinus tachycardia, blurred vision.
269
Features of severe poisoning [4]
arrhythmias seizures metabolic acidosis coma
270
ECG changes in TCA OD [3]
sinus tachycardia widening of QRS prolongation of QT interval
271
What is a widening of 100ms QRS and a widening of 160ms associated with? [2]
Widening of QRS > 100ms is associated with an increased risk of seizures whilst QRS > 160ms is associated with ventricular arrhythmias
272
What drugs should be avoided to manage arrhythmias in TCA OD? [4]
``` + class 1a (e.g. Quinidine) and class Ic antiarrhythmics (e.g. Flecainide) are contraindicated as they prolong depolarisation class III drugs such as amiodarone should also be avoided as they prolong the QT interval response to lignocaine is variable and it should be emphasized that correction of acidosis is the first line in management of tricyclic induced arrhythmias ```
273
What can given to reduce toxicity for TCA OD? [1]
intravenous lipid emulsion is increasingly used to bind free drug and reduce toxicity
274
Summarise Tx for TCA OD [3]
1. IV bicarbonate 2. Antiarrhythmia drugs 3. IV lipid emulsion
275
Patient Dx with dry ARMD, what would indicate neo-proliferative changes of this patient's condition? [2]
Decreasing vision over months with metamorphopsia and central scotoma should cause high suspicion of wet age-related macular degeneration
276
What is central scotoma? [1]
Loss of central vision
277
What does central scrotoma result from? [1]
results from neovascularisation under the retina [choroidal neovascularisation] and subsequent haemorrhage
278
Cherry red spot against pale retina fundoscopy [1]
central retinal artery occlusion
279
Bayonetting of retinal vessels fundoscopy [1]
open-angle glaucoma
280
What is hypopyon associated with? [1]
Hypopyon is incorrect. This describes an accumulation of neutrophils in the anterior chamber of the eye and is most commonly associated with anterior uveitis
281
Why is it important to Tx alcohol withdrawal promptly? [1]
Can lead to delirium tremens -> life-threatening
282
What is Wernicke's encephalopathy? [3]
triad of ataxia, confusion and ophthalmoplegia
283
How is Wernicke's encephalophy managed? [1]
IV thiamine
284
Which NT does chronic alcoholism enhance? [2]
chronic alcohol consumption enhances GABA mediated inhibition in the CNS (similar to benzodiazepines) and inhibits NMDA-type glutamate receptors
285
When do features start of acute alcohol withdrawal? [2]
symptoms start at 6-12 hours: tremor, sweating, tachycardia, anxiety
286
When do peak Sx start of alcohol withdrawal? [2]
peak incidence of seizures at 36 hours | peak incidence of delirium tremens is at 48-72 hours
287
Sx of delirium tremens [3]
coarse tremor, confusion, delusions, auditory and visual hallucinations, fever, tachycardia
288
How should patients with complex history of withdrawals be Mx? [1]
patients with a history of complex withdrawals from alcohol (i.e. delirium tremens, seizures, blackouts) should be admitted to hospital for monitoring until withdrawals stabilised
289
1st line Rx for alcohol withdrawal [1]
long-acting benzodiazepines e.g. chlordiazepoxide or diazepam. [carbamazepine can also be effective]
290
What may be preferable in patients with AW with hepatic failure? [1]
Lorazepam [short-acting benzo]
291
What should be organised when there are signs of an atypical UTI in infants under 6m? [1]
US should be organised
292
Features of atypical UTI [7]
``` Seriously ill Poor urine flow Abdominal or bladder mass Raised creatinine Septicaemia Failure to respond to treatment with suitable antibiotics within 48 hours Infection with non-E. coli organisms ```
293
Is abdominal pain a feature of atypical UTI? [1]
Yes
294
Presentation in childhood of UTI in infants vs younger children vs older children vs upper UTI [4]
infants: poor feeding, vomiting, irritability younger children: abdominal pain, fever, dysuria older children: dysuria, frequency, haematuria features which may suggest an upper UTI include: temperature > 38ºC, loin pain/tenderness
295
NICE guidelines for checking urine simple in a child [3]
if there are any symptoms or signs suggestive or a UTI with unexplained fever of 38°C or higher (test urine after 24 hours at the latest) with an alternative site of infection but who remain unwell (consider urine test after 24 hours at the latest)
296
Urine collection method for UTI in children [3]
clean catch is preferable if not possible then urine collection pads should be used cotton wool balls, gauze and sanitary towels are not suitable invasive methods such as suprapubic aspiration should only be used if non-invasive methods are not possible
297
How should infants under3m be Tx with a UTI? [1]
infants less than 3 months old should be referred immediately to a paediatrician
298
Which sages is cervical screening offered? [1]
25-49 years
299
How common is cervical screening 25-49 years? [1]
3-yearly
300
How common is cervical screening 50-64 years?
5y
301
Which two special situations do women delay their cervical smear? [2]
cervical screening in pregnancy is usually delayed until 3 months post-partum unless missed screening or previous abnormal smears. women who have never been sexually active have very low risk of developing cervical cancer therefore they may wish to opt-out of screening
302
How can HPV be transmitted? [1]
Oral or genital contact
303
What is the causative virus for cervical cancer? [1]
HPV
304
What is now used instead of Pap smears? [1]
liquid-based cytology (LBC)