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
Q

What is the risk of GBS carriage in new pregnancy if they’ve already had it previous one? [1]

A

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%

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26
Q

When should women have swabs for GBS? [1]

A

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

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27
Q

when should women be given IAP? [1]

A

women with a pyrexia during labour (>38ºC) should also be given IAP

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28
Q

Positive p24 and antibody test for HIV, what should happen? [2]

A
  • started on anti-retroviral treatment today

- repeat HIV p24 and antibody in 12w time

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29
Q

When can post-exposure prophylaxis be commenced? [1]

A

Can only be started 72 hours after possible exposure [i.e. recent high risk sex]

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30
Q

How common is HIV seroconversion symptomatic in HIV patients? [1]

A

60-80%

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31
Q

Typical presentation of HIV seroconversion [1]

A

Glandular type fever illness

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32
Q

When does HIV seroconversion typically occur? [1]

A

3-12w after infection

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33
Q

Features of HIV seroconversion [3]

A
sore throat
lymphadenopathy
malaise, myalgia, arthralgia
diarrhoea
maculopapular rash
mouth ulcers
rarely meningoencephalitis
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34
Q

When do HIV antibodies develop? [1]

A

may not be present in early infection, but most people develop antibodies to HIV at 4-6 weeks but 99% do by 3 months

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35
Q

When does p24 antigen become testable? [2]

A

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

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36
Q

When should a HIV test be offered for possible exposure? [1]

A

testing for HIV in asymptomatic patients should be done at 4 weeks after possible exposure

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37
Q

What is the standard for HOV diagnosis and screening? [2]

A

combination tests (HIV p24 antigen and HIV antibody) are now standard for the diagnosis and screening of HIV

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38
Q

Most common CXR finding in PE? [1]

A

normal CXR

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39
Q

How common are tachypnea, crackles, tachycardia, fever in PE? [4]

A

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%

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40
Q

What is recommended as initial lung-imaging modality for non-massive PE? [1]

A

CTPA scan

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41
Q

Advantages of CTPA over V/Q scan [3]

A

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

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42
Q

If CTPA negative, are further tests required?

A

No, also no need Ix

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43
Q

When is V/Q scanning appropriate? [4]

A

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?

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44
Q

Sensitivity and specificity of D-dimers [1]

A

95-98%

Poor specificity

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45
Q

ECG changes in PE [3]

A
  • 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
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46
Q

How common is S1Q3T3? [1]

A

20% only of PE patients

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47
Q

Why is CXR ordered in PE? [1]

A

to r/o other causes

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48
Q

What might be found CXR in PE? [2]

A

Wedge-shaped opacification

Typically normal though

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49
Q

Sensitivity and specificity of V/Q scan [2]

A

sensitivity of around 75% and specificity of 97%

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50
Q

What type of brain injury is a lucid interval associated with? [1]

A

EDH

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51
Q

Types of primary brain injury [2]

A

Focal [contusion/haematoma] or diffuse [diffuse axonal injury]

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52
Q

How can diffuse axonal injuries occur? [1]

A

diffuse axonal injury occurs as a result of mechanical shearing following deceleration, causing disruption and tearing of axons

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53
Q

Where do contusions occur? [1]

A

contusions may occur adjacent to (coup) or contralateral (contre-coup) to the side of impact

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54
Q

When do secondary brain injuries occur? [4]

A

secondary brain injury occurs when cerebral oedema, ischaemia, infection, tonsillar or tentorial herniation exacerbates the original injury

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55
Q

What happens to the brain in secondary brain injuries? [2]

A

The normal cerebral auto regulatory processes are disrupted following trauma rendering the brain more susceptible to blood flow changes and hypoxia

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56
Q

What is Cushing reflex and when does it occur? [3]

A

the Cushings reflex (hypertension and bradycardia) often occurs late and is usually a pre terminal event

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57
Q

Where do EDH typically occur? [2]

A

The majority of epidural haematomas occur in the temporal region where skull fractures cause a rupture of the middle meningeal artery.

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58
Q

Features of EDH [2]

A

Raised ICP

Some patients have lucid interval

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59
Q

When do EDH typically occur? [1]

A

Often results from acceleration-deceleration trauma or a blow to the side of the head

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60
Q

Where do SDH typically occur? [1]

A

Most commonly occur around the frontal and parietal lobes.

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61
Q

RFs for SDH [3]

A

Risk factors include old age, alcoholism and anticoagulation.

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62
Q

Compare SDH to EDH [2]

A

Slower onset of symptoms than a epidural haematoma. There may be fluctuating confusion/consciousness

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63
Q

Classically, how does a subarachnoid haemorrhage present? [1]

A

Classically causes a sudden occipital headache.

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64
Q

When does SaH commonly occur? [2]

A

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

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65
Q

What is a intracerebral haematoma? [1]

A

An intracerebral (or intraparenchymal) haemorrhage is a collection of blood within the substance of the brain

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66
Q

Causes/RF of ICH [5]

A

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).

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67
Q

Why is it crucial to obtain a CT in head in all stroke patients prior to thrombolysis? [2]

A

Patients will present similarly to an ischaemic stroke in ICH
Or will present with decreased LOC

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68
Q

Blood profile of a patient with anaemia of chronic disease [4]

A

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

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69
Q

Three distinct pathological processes in iron profile of anaemia of chronic disease [3]

A

reduced iron release from marrow, inadequate secretion of EPO for erythropoiesis and reduced red cell survival

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70
Q

Why is ferritin raised in chronic inflammation? [1]

A

Ferritin is an acute phase reactant and therefore raised in states of chronic inflammation, as is likely to be the case in this patient.

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71
Q

Why are platelets raised in chronic anaemia? [1]

A

The platelets are raised due to a reactive thrombocytosis in the presence of inflammation.

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72
Q

Blood profile of iron defieicny anaemia [3]

A

Iron deficiency anaemia causes a microcytic anaemia, low ferritin and a raised TIBC

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73
Q

Hereditary haemochromatosis blood picture [3]

A

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.

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74
Q

What does sidroblastic anaemias typically cause blood profile? [2]

A

Sideroblastic anaemia usually causes a microcytic anaemia with raised serum iron levels.

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75
Q

Causes of normocytic anaemias [5]

A
anaemia of chronic disease
chronic kidney disease
aplastic anaemia
haemolytic anaemia
acute blood loss
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76
Q

What should be offered to patients with intrahepatic cholestasis and why? [2]

A

Intrahepatic cholestasis of pregnancy increases the risk of stillbirth; therefore induction of labour is generally offered at 37-38 weeks gestation

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77
Q

how common is intrahepatic cholestasis in pregnancy? [1]

A

1% in the UK

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78
Q

Features of intrahepatic cholestasis of pregnancy [3]

A

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

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79
Q

Mx of cholestasis of pregnancy [3]

A

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

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80
Q

How common is recurrence of intrahepatic cholestasis of pregnancy? [1]

A

Recurrence of intrahepatic cholestasis of pregnancy is 45-90% in subsequent pregnancies.

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81
Q

Presentation of biliary colic vs cholecystitis [4]

A

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.

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82
Q

What is ERCP procedure used for? [1]

A

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

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83
Q

Signs of an obstructing stone include what? [1]

A

Signs of an obstructing stone would include jaundice, of which there is no mention here

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84
Q

What is biliary colic caused by? [1]

A

Biliary colic is caused by gallstones passing through the biliary tree.

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85
Q

RFs for biliary colic [4]

A

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

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86
Q

Other notable RFs for biliary colic [4]

A

diabetes mellitus
Crohn’s disease
rapid weight loss e.g. weight reduction surgery
drugs: fibrates, combined oral contraceptive pill

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87
Q

Simple PP of biliary colic [3]

A

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

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88
Q

Features of biliary colic [3]

A

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

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89
Q

Ix for biliary colic [1]

A

ultrasound

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90
Q

Mx of biliary colic [1]

A
  • elective laparoscopic cholecystectomy
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91
Q

How common is it to have gallstones in the common bile duct? [1]

A

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

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92
Q

Possible Cx other than biliary colic of a gallstone [5]

A
acute cholecystitis: the most common complication
ascending cholangitis
acute pancreatitis
gallstone ileus
gallbladder cancer
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93
Q

What is most likely to be observed in the synovial fluid taken from a patients knee with reactive arthritis? [2]

A

Sterile synovial fluid with a high WCC

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94
Q

24 y/o painful right knee, lethargy, feverish Sx, PMH includes chlaydia infection 2w previously. Dx? [1]

A

Septic arthritis

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95
Q

Define reactive arthritis [3]

A

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

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96
Q

What type of WBCs will be seen in synovial fluid of patient with reactive arthritis? [1]

A

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).

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97
Q

When are negatively birefringent crystals seen in pts? [2]

A

commonly seen in calcium pyrophosphate deposition (pseudogout).

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98
Q

Positively birefringent crystals seen commonly when? [1]

A

Gout

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99
Q

What are smears done to test? [1]

A

Cervical cancer

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100
Q

What should happen if 2 consecutive inadequate samples taken cervical smear? [1]

A

Refer to colposcopy

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101
Q

Which system does the cervical cancer screening employ currently? [2]

A

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.

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102
Q

If patient has negative hrHPV, what should you do? [5]

A

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

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103
Q

If hrHPV is positive and cytology is abnormal, what should be next line Mx? [1]

A

if the cytology is abnormal → colposcopy

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104
Q

If cytology is normal, but hrHPV is abnormal, what should be done? [1]

A

if the cytology is normal (i.e. hrHPV +ve but cytologically normal) the test is repeated at 12 months

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105
Q

If cervical sample is inadequate [2]

A

repeat the sample within 3 months

if two consecutive inadequate samples then → colposcopy

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106
Q

Inherited causes of thrombophilia [5]

A

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
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107
Q

Prevalence and RR of VTE in factor V Leiden [heterozygous]

A

prevalence 5%, relative risk of VTE is 4

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108
Q

Prevalence and RR of VTE in protein C deficiency

A

0.3% and RR is 10

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109
Q

Acquired causes of thrombophilia [2]

A

Antiphospholipid syndrome

Drugs
the combined oral contraceptive pill

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110
Q

What is Hodgkins lymphoma? [2]

A

Hodgkin’s lymphoma is a malignant proliferation of lymphocytes characterised by the presence of the Reed-Sternberg cell

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111
Q

When is Hodgkin’s lymphoma most common? [1]

A

It has a bimodal age distributions being most common in the third and seventh decades

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112
Q

What is the most common type of HL? [1]

A

nodular sclerosing

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113
Q

Features of nodular sclerosing HL [3]

A

More common in women. Associated with lacunar cells

Good prognosis

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114
Q

Which HL type has best prognosis, which has the worst prognosis? [2]

A

Lymphocyte predominant [5%] best prognosis, lymphocyte depleted [rare] worst prognosis

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115
Q

What is HSP? [2]

A

HSP is a IgA mediated small vessel vasculitis

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116
Q

When is HSP seen? [1]

A

Usually seen in children following an infection

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117
Q

Features of HSP [4]

A

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

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118
Q

Tx for HSP [2]

A

analgesia for arthralgia
treatment of nephropathy is generally supportive. There is inconsistent evidence for the use of steroids and immunosuppressants

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119
Q

Prognosis of HSP [2]

A

usually excellent, HSP is a self-limiting condition, especially in children without renal involvement
around 1/3rd of patients have a relapse

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120
Q

Where is Legionnaire’s disease typically contracted from? [1]

A

It typically colonizes water tanks and hence questions may hint at air-conditioning systems or foreign holidays.

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121
Q

Is Legionaires transmittable? [1]

A

No not person-to-person

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122
Q

Features of Legionella [8]

A
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
Q

Are lymphocytes raised/depressed in Legionella? [1]

A

Depressed -> lymphopaenia not lymphocytosis

124
Q

Dx of Legionella [1]

A

Urinary antigen

125
Q

Tx of Legionella [1]

A

Tx with erythromycin/clarithromycin

126
Q

Similarities between Legionella and Mcyoplasma pneumonia [5]

A
Atypical presentation
Flu-like Sx
Dry cough
Deranged LFTs
treat with macrolide [e.g. erhyromycin]
127
Q

Which tool is used for postnatal depression? [2]

A

Edinburgh scale [or the PHQ-9]

128
Q

GAD-7 questionnaire used for? [1]

A

anxiety

129
Q

Bishop score [1]

A

informing the induction of labour

130
Q

FAST and CAGE score [2]

A

alcoholism

131
Q

What are the baby-blues? [4]

A
  • 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
Q

How common is PND? [1]

A

Typically 10% of mothers

133
Q

When does PND start? [1]

A

Most within a month, typically peaking at around 3m

134
Q

Sx of PND [1]

A

Similar to depression

135
Q

Mx of PND [3]

A

CBT may be beneficial

Certain SSRIs such as sertraline/paroxetine if Sx severe

136
Q

Are SSRIs harmful to the baby? [1]

A

Secreted breast milk, but not harmful

137
Q

Features of puerperal psychosis [2]

A

Features include severe swings in mood (similar to bipolar disorder) and disordered perception (e.g. auditory hallucinations)

138
Q

How common is puerperal psychosis, and when does onset occur? [2]

A

Affects approximately 0.2% of women

Onset usually within the first 2-3 weeks following birth

139
Q

Mx of puerperal psychosis [1]

A

Admission to hospital is usually required

140
Q

Risk of recurrence of puerperal psychosis [1]

A

There is around a 25-50% risk of recurrence following future pregnancies

141
Q

What is glandular fever also known as? [1]

A

Infectious mononucleosis

142
Q

What is infectious mononucleosis caused by in 90% of cases? [1]

A

EBV [also know as human herpesvirus 4]

143
Q

Other causes of glandular fever [2]

A

Cytomegalovirus

144
Q

Population most common in IM [1]

A

Adolescents and young adults

145
Q

What is the classic triad seen in 98% of IM patients? [3]

A

Sore throat
Lymphadenopathy
Pyrexia

146
Q

Difference in lymphadenopathy of IM compared to tonsillitis [1]

A

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
Q

Other features of IM [3]

A

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
Q

What happens to patients 99% of patients treated with ampicillin/amoxicillin whilst they have IM? [1]

A

a maculopapular, pruritic rash develops in around 99% of patients who take ampicillin/amoxicillin whilst they have infectious mononucleosis

149
Q

How to Dx IM? [1]

A

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
Q

Mx of glandular fever [3]

A

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
Q

How should people exposed to a patient with confirmed bacterial meningitis be Tx? [1]

A

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
Q

In a young student, what is the common causative organism for bacterial meningitis? [2]

A

Neisseria meningitidis and Streptococcus pneumoniae

153
Q

Ix for meningitis [8]

A
Investigations suggested by NICE
full blood count
CRP
coagulation screen
blood culture
whole-blood PCR
blood glucose
blood gas

Lumbar puncture

154
Q

When should you not do an LP in meningitis? [1]

A

Signed of raised ICP

155
Q

If patient is waiting and is meningococcal disease is suspected, what should be given? [1]

A

intramuscular benzylpenicillin may be given, as long as this doesn’t delay transit to hospital.

156
Q

Initial empirical therapy for patients aged 3 to 50 y/ [1]o

A

IV cefotaxime [or ceftriaxone]

157
Q

Rx for patient with confirmed IV meningococcal meningitis [1]

A

Intravenous benzylpenicillin or cefotaxime (or ceftriaxone)

158
Q

What should also be given alongside abx for meningitis? When should this be withheld? [5]

A
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
Q

Which drug to give if patient has hypersensitivity to penicillin or cephalosporins? [1]

A

Chloramphenicol

160
Q

Close contact how many days before onset meningitis prophylaxis? [1]

A

7 days

161
Q

Which drug should be given close contact meningitis 7 days previously? [2]

A

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
Q

Two main ways of AAA presenting [2]

A

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
Q

Features of an AAA

A

central abdominal pain radiating to the back
pulsatile mass in the abdomen
patients may be shocked (hypotension, tachycardic)

164
Q

What is the single most important step definitive Mx of patient’s condition with AAA? [1]

A

Seek immediate vascular review

165
Q

how is an AAA typically diagnosed? [1]

A

The diagnosis is clinical, these patients are not stable enough for a CT scan etc to confirm the diagnosis.

166
Q

What would inferior STEMI look like on an ECG? [1]

A

An inferior STEMI would cause ST elevation in leads II, III and aVF

167
Q

What would lateral STEMI look like on an ECG? [1]

A

ST elevation in leads I, aVL and V5-V6

168
Q

What would NSTEMI look like on an ECG? [3]

A

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
Q

What would LVH show on an ECG? [2]

A

sum of S wave in V1 and R wave in V5 or V6 exceeds 40 mm

170
Q

What would RVH show on an ECG? [4]

A

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
Q

What is the commonest skin disorder in pregnancy? [1]

A

Atopic eruption in pregnancy

172
Q

Features of atopic eruption pregnancy [2]

A

it typically presents as an eczematous, itchy red rash.

no specific treatment is needed

173
Q

Features of polymorphic eruption of pregnancy [3]

A

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
Q

Features of pemphigoid gestations [4]

A

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
Q

What type of drug is lidocaine? [1]

A

Amide

176
Q

How does it work and does this mean it’s used for? [2]

A

Local anaesthetic and less commonly anti arrhythmic [affects Na channels in the axon]

177
Q

How can lidocaine toxicity occur? [2]

A

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
Q

How can local anaesthetic toxicity be treated? [1]

A

Local anesthetic toxicity can be treated with IV 20% lipid emulsion

179
Q

Concentration of cocaine used clinically [1]

A

It is supplied for clinical use in concentrations of 4 and 10%

180
Q

how is cocaine applied? [1]

A

It may be applied topically to the nasal mucosa

181
Q

How does cocaine act? [1]

A

It has a rapid onset of action and has the additional advantage of causing marked vasoconstriction.

182
Q

Systemic effects of cocaine [1]

A

Its systemic effects also include cardiac arrhythmias and tachycardia.

183
Q

When is it used medicine? [1]

A

Apart from its limited use in ENT surgery it is otherwise used rarely in mainstream surgical practice.

184
Q

How does bupivacaine work? [2]

A

Bupivacaine binds to the intracellular portion of sodium channels and blocks sodium influx into nerve cells, which prevents depolarization.

185
Q

Advantage of bupivacaine over lignocaine [1]

A

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
Q

When is Bupivacaine contra-indicated and what is used as a replacement? [2]

A

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
Q

When is Prilocaine used? [1]

A

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
Q

Why is adrenaline sometimes added to local anaesthetics? [2]

A

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
Q

When is adrenaline CI for use with local anaesthetics? [1]

A

It is contra indicated in patients taking MAOI’s or tricyclic antidepressants.

190
Q

What type of incontinence is caused by bladder still palpable after urination? [1]

A

think retention with urinary overflow

191
Q

Most common cause of urinary overflow incontinence [1]

A

Prostate problems

192
Q

Causes of urinary overflow incontinence in a women [3]

A

Other causes can include nerve damage causing a neurogenic bladder such as complication of diabetics, chronic alcoholics or surgery to the pelvic area.

193
Q

Sx of overactive balder [1]

A

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
Q

What is mixed urinary incontinence? [2]

A

urge and stress incontience combined

195
Q

RFs for urinary incontinence [5]

A
advancing age
previous pregnancy and childbirth
high body mass index
hysterectomy
family history
196
Q

OAB definition [1]

A

overactive bladder (OAB)/urge incontinence: due to detrusor overactivity

197
Q

Stress classification [1]

A

leaking small amounts when coughing or laughin

198
Q

overflow incontinence [1]

A

overflow incontinence: due to bladder outlet obstruction, e.g. due to prostate enlargement

199
Q

Initial Ix for incontinence [4]

A

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
Q

Mx of urge incontinence [3]

A

bladder retraining
bladder stabilising drugs
mirabegron

201
Q

How long should bladder retraining take? [1]

A

lasts for a minimum of 6 weeks, the idea is to gradually increase the intervals between voiding)

202
Q

Drugs to give for bladder stabilising effects in urge incontinence [3]

A

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
Q

Which drug should be given to frail older women with incontinence for bladder stabilising? [1]

A

mirabegron (a beta-3 agonist) may be useful if there is concern about anticholinergic side-effects in frail elderly patients

204
Q

Stress incontinence Mx [3]

A
  • Pelvic floor muscle training
  • Surgical procedures [e.g. retropubic mid-urethral tap procedures]
  • Duloxetine if declined surgical procedures
205
Q

Pelvic floor muscle training how is it done? [1]

A

NICE recommend at least 8 contractions performed 3 times per day for a minimum of 3 months

206
Q

How does duloxetine work for women with stress incontinence? [2]

A

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
Q

How does presbycusis present? [1]

A

Presbycusis presents with bilateral high-frequency hearing loss

208
Q

What is presbycusis? [1]

A

Age related sensorineural deafness, initially affecting high-frequency tones. Particularly in noisy envirnoments.

209
Q

Why type of conduction is greater in sensoryneural hearing loss? [1]

A

Air conduction is superior to bone conduction

210
Q

Epidemiology of presbycusis [3]

A

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
Q

Causes of presbycusis [3]

A

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
Q

Presentation of presbycusis [3]

A

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
Q

Ix can be done for presbycusis, what will they show? [8]

A

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
Q

Audiometry in presbycusis [1]

A

Bilateral sensorineural pattern hearing loss

215
Q

Mx of acute pancreatitis? [1]

A

Fluids and analgesia [Abx should not be routinely Rx]

216
Q

What is flank discolouration a sign of? [1]

A

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
Q

What fluids should be offered for acute pancreatitis? [3]

A

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
Q

Which analgesia commonly given acute pancreatitis? [1]

A

pain may be severe so this is a key priority of care

intravenous opioids are normally required to adequately control the pain

219
Q

How should patients have their nutrition? [3]

A
  • 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
Q

What is the role of antibiotics in acute pancreatitis? [2]

A

NICE state the following: ‘Do not offer prophylactic antimicrobials to people with acute pancreatitis’
potential indications include infected pancreatic necrosis

221
Q

What is the role of surgery in acute pancreatitis? [4]

A

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
Q

What is erythema ab igne? [1]

A

Erythema ab igne is a skin disorder caused by over exposure to infrared radiation.

223
Q

Characteristic features of erythema ab igne [4]

A

Characteristic features include reticulated, erythematous patches with hyperpigmentation and telangiectasia.

224
Q

Typical history of erythema ab ignore [1]

A

A typical history would be an elderly women who always sits next to an open fire.

225
Q

Why is it important to Tx erythema ab igne? [1]

A

Squamous cell skin cancer may develop

226
Q

When is a nuchal translucency performed? [1]

A

11-13w

227
Q

Causes of increased nuchal transluscency [3]

A

Down’s syndrome
congenital heart defects
abdominal wall defects

228
Q

Causes of hyperchogenic bowel on a NL [3]

A

cystic fibrosis
Down’s syndrome
cytomegalovirus infection

229
Q

What can prolonged, untreated secondary hyperparathyroidism lead to? [1]

A

Tertiary hyperparathyroidism

230
Q

Signs of hypercalcamia [5]

A

Worsening fatigue, thirst, anorexia, general aches and pains

231
Q

Hormone profile or primary vs secondary vs tertiary hyperparathyroidism [3]

A

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
Q

Clinical features of primary vs secondary vs tertiary hyperparathyroidism [3]

A

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
Q

Cause of primary vs secondary vs tertiary hyperparathyroidism [3]

A

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
Q

Ddx of hyperparathyoidism [1]

A

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
Q

Tx for primary hyperparathyroidism [3]

A

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
Q

Mx of secondary hyperparathyroidism [4]

A

Usually managed with medical therapy.

Indications for surgery in secondary (renal) hyperparathyroidism:
Bone pain
Persistent pruritus
Soft tissue calcifications

237
Q

Mx of tertiary hyperparathyroidism [2]

A

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
Q

Patients Dx with pneumonia who have COPD should be given what? [1]

A

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
Q

Primary vs secondary care setting for looking after patient with pneumonia

A

Primary
- CRB65
Secondary
- CURB65

240
Q

Criteria of CURB65

A
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
Q

Recommendation for CURB65 score

A
0-1 = consider home-based care
2+ = consider hospital-based care
3+ = consider intensive care
242
Q

Ix for patients with pneumonia who have COPD

A

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
Q

First-line Mx of low-severity CAP [3]

A

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
Q

Mx of moderate to high-severity CAP [3]

A

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
Q

How does critical limb ischaemia typically present? [2]

A

Critical limb ischaemia presents as pain at rest for greater than 2 weeks, often at night, not helped by analgesia

246
Q

What is critical limb ischaemia caused by? [1]

A

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
Q

What is CLI initially? [1]

A

Initially, peripheral arterial disease presents as intermittent claudication. However, as the disease progresses, pain becomes present at rest.

248
Q

How to differentiate between CLI and acute limb ischaemia? [1]

A

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
Q

Why is acute limb ischaemia an emergency? [1]

A

However, if not treated promptly, this patient may develop acute limb ischaemia which is a limb-threatening emergency.

250
Q

Features of CLI [3]

A

However, if not treated promptly, this patient may develop acute limb ischaemia which is a limb-threatening emergency.

251
Q

What do patients often report with CLI? [1]

A

hanging their legs out of bed at night

252
Q

What is an ABPI for CLI? [1]

A

Over 0.5

253
Q

What is pernicious anaemia? [2]

A

Pernicious anaemia is an autoimmune disorder affecting the gastric mucosa that results in vitamin B12 deficiency.

254
Q

Causes of B12 deficiency [3]

A

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
Q

PP of pernicious anaemia

A

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
Q

Why is vitamin B12 important in bodies? [2]

A

vitamin B12 is important in both the production of blood cells and the myelination of nerves → megaloblastic anaemia and neuropathy

257
Q

RFs for pernicious anaemia [3]

A

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
Q

Features of pernicious anaemia [3]

A

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
Q

Ix for pernicious anaemia [3]

A

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
Q

Mx of B12 deficiency [2]

A

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
Q

How vitamin B12 is replaced in pernicious anaemia with no neurological features? [2]

A

3 injections per week for 2w, followed by 3 monthly Tx of vitamin B12 injections

262
Q

Cx other than haematological and neurological features [1]

A

increased risk of gastric cancer

263
Q

When to consider gastric lavage for tricyclic OD? What else can be given? [2]

A

Consider gastric OD only within 1 hour of potentially fatal OD
50g of charcoal if within 1h ingestion

264
Q

What to give to treat tricyclic OD? [1]

A

IV sodium bicarbonate [50ml of 8.4%]

265
Q

When to give sodium bicarbonate in OD? [4]

A

pH <7.1
QRS >160 ms
Arrhythmias
Hypotension

266
Q

When is IV adenosine given? [1]

A

Adenosine is used in the management of supraventricular tachycardia.

267
Q

Which tricyclics are particularly dangerous? [1]

A

Overdose of tricyclic antidepressants is a common presentation to emergency departments. Amitriptyline and dosulepin (dothiepin) are particularly dangerous in overdose.

268
Q

What are early features related to tricyclic OD? [2]

A

Early features relate to anticholinergic properties: dry mouth, dilated pupils, agitation, sinus tachycardia, blurred vision.

269
Q

Features of severe poisoning [4]

A

arrhythmias
seizures
metabolic acidosis
coma

270
Q

ECG changes in TCA OD [3]

A

sinus tachycardia
widening of QRS
prolongation of QT interval

271
Q

What is a widening of 100ms QRS and a widening of 160ms associated with? [2]

A

Widening of QRS > 100ms is associated with an increased risk of seizures whilst QRS > 160ms is associated with ventricular arrhythmias

272
Q

What drugs should be avoided to manage arrhythmias in TCA OD? [4]

A
\+ 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
Q

What can given to reduce toxicity for TCA OD? [1]

A

intravenous lipid emulsion is increasingly used to bind free drug and reduce toxicity

274
Q

Summarise Tx for TCA OD [3]

A
  1. IV bicarbonate
  2. Antiarrhythmia drugs
  3. IV lipid emulsion
275
Q

Patient Dx with dry ARMD, what would indicate neo-proliferative changes of this patient’s condition? [2]

A

Decreasing vision over months with metamorphopsia and central scotoma should cause high suspicion of wet age-related macular degeneration

276
Q

What is central scotoma? [1]

A

Loss of central vision

277
Q

What does central scrotoma result from? [1]

A

results from neovascularisation under the retina [choroidal neovascularisation] and subsequent haemorrhage

278
Q

Cherry red spot against pale retina fundoscopy [1]

A

central retinal artery occlusion

279
Q

Bayonetting of retinal vessels fundoscopy [1]

A

open-angle glaucoma

280
Q

What is hypopyon associated with? [1]

A

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
Q

Why is it important to Tx alcohol withdrawal promptly? [1]

A

Can lead to delirium tremens -> life-threatening

282
Q

What is Wernicke’s encephalopathy? [3]

A

triad of ataxia, confusion and ophthalmoplegia

283
Q

How is Wernicke’s encephalophy managed? [1]

A

IV thiamine

284
Q

Which NT does chronic alcoholism enhance? [2]

A

chronic alcohol consumption enhances GABA mediated inhibition in the CNS (similar to benzodiazepines) and inhibits NMDA-type glutamate receptors

285
Q

When do features start of acute alcohol withdrawal? [2]

A

symptoms start at 6-12 hours: tremor, sweating, tachycardia, anxiety

286
Q

When do peak Sx start of alcohol withdrawal? [2]

A

peak incidence of seizures at 36 hours

peak incidence of delirium tremens is at 48-72 hours

287
Q

Sx of delirium tremens [3]

A

coarse tremor, confusion, delusions, auditory and visual hallucinations, fever, tachycardia

288
Q

How should patients with complex history of withdrawals be Mx? [1]

A

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
Q

1st line Rx for alcohol withdrawal [1]

A

long-acting benzodiazepines e.g. chlordiazepoxide or diazepam.
[carbamazepine can also be effective]

290
Q

What may be preferable in patients with AW with hepatic failure? [1]

A

Lorazepam [short-acting benzo]

291
Q

What should be organised when there are signs of an atypical UTI in infants under 6m? [1]

A

US should be organised

292
Q

Features of atypical UTI [7]

A
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
Q

Is abdominal pain a feature of atypical UTI? [1]

A

Yes

294
Q

Presentation in childhood of UTI in infants vs younger children vs older children vs upper UTI [4]

A

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
Q

NICE guidelines for checking urine simple in a child [3]

A

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
Q

Urine collection method for UTI in children [3]

A

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
Q

How should infants under3m be Tx with a UTI? [1]

A

infants less than 3 months old should be referred immediately to a paediatrician

298
Q

Which sages is cervical screening offered? [1]

A

25-49 years

299
Q

How common is cervical screening 25-49 years? [1]

A

3-yearly

300
Q

How common is cervical screening 50-64 years?

A

5y

301
Q

Which two special situations do women delay their cervical smear? [2]

A

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
Q

How can HPV be transmitted? [1]

A

Oral or genital contact

303
Q

What is the causative virus for cervical cancer? [1]

A

HPV

304
Q

What is now used instead of Pap smears? [1]

A

liquid-based cytology (LBC)