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MSRA > Everything else - Passmed > Flashcards

Everything else - Passmed Flashcards

1
Q

Risk factors for SBOS (Small bowel bacterial overgrowth syndrome)?

A
  • Neonates with congenital gastrointestinal abnormalities
  • Scleroderma
  • Diabetes Mellitus
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2
Q

Key investigations for SBOS (small bowel bacterial overgrowth syndrome)?

A
  • Hydrogen breath test
  • Sometimes give a course of antibiotics as a diagnostic trial
  • Small bowel aspiration and culture - this is used less often as invasive and results are often difficult to reproduce
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3
Q

What is the management of SBOS (small bowel bacterial overgrowth syndrome)?

A

Antibiotic therapy - rifaximin

Note co-amox or metronidazole are also effective in most patients

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4
Q

Give 2 examples of GLP-1 mimetics

A

Liraglutide
Exenatide

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5
Q

Liraglutide and exenatide belong to which class of diabetes medications?

A

GLP-1 mimetics

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6
Q

What is a good side effect of GLP-1 mimetics?

A

Weight loss

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7
Q

What is a good benefit of Liraglutide over Exenatide?

A

Liraglutide only needs to be given once a day

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8
Q

When patient is already on metformin and a sulfonylurea, in what situations according to NICE can we add on exenatide (GLP-1 mimetic)?

A
  • When BMI > / = 35 kg/m2 in people of european descent and there are problems associated with high weight or
  • BMI < 35 kg/m2 and insulin is unacceptable because of occupational implications or weight loss would benefit other comorbidities
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9
Q

What targets for HbA1C and weight loss are set by NICE to justify the ongoing prescription of GLP-1 mimetics?

A

> 11 mmol/mol (1%) reduction in HbA1C and 3% weight loss after 6 months to justify the ongoing prescription of GLP-1 mimetics

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10
Q

What is the mechanism of action of DPP-4 inhibitors?

A

They increase the level of incretins (GLP-1 and GIP) by decreasing their peripheral breakdown

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11
Q

When are DPP-4 inhibitors preferable to thiazolidinediones?

A

If further weight gain would cause significant problems, a thiazolidinedione is contraindicated or the person has a poor response to thiazolidinediones

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12
Q

Give two examples of DPP-4 inhibitors?

A

Sitagliptin
Vildagliptin

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13
Q

True or false DPP-4 inhibitors e.g. sitagliptin cause weight gain?

A

False

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14
Q

In heart failure, what are the dinidcations for:
1) Cardiac resynchronisation therapy?
2) Implantable cardiac defibrillator (ICD)?

A

1) Cardiac resynchronisation therapy
- Heart failure NYHA class III
- Left ventricular dysfunction
- Ejection fraction < 35%
- QRS duration > 120ms

2) Implantable cardiac defibrillator (ICD)
- Symptoms no more than NYHA class III
- Ejection fraction < 35%
- Sustained ventricular tachycardia

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15
Q

What type of pacing is done in chronic heart failure?

A

Biventricular pacing

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16
Q

Most common cause of CAP (organism)?

A

Streptococcus pneumoniae

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17
Q

Predisposing influenza predisposes to pneumonia related to which organism?

A

Staph Aureus

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18
Q

Which anticoagulation is absolutely contra-indicated in pregnancy?

A

Warfarin - as it is teratogenic

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19
Q

Which anticoagulant is recommended first line for VTE treatment in pregnancy?

A

Low molecular weight heparin - it has a preferable safety profile as compared to unfractionated heparin and is equally effective

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20
Q

Target INR is higher in atrial or mitral valve metallic replacements?

A

Higher in mitral valve replacements

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21
Q

1) VTE treatment with warfarin what target INR is usually set?

2) What about in AF?

3) What about in metallic heart valves?

A

1) VTE treatment - usually 2.5 target, if recurrent 3.5

2) Atrial fibrillation target INR = 2.5

3) Mechanical heart valves = 3-3.5

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22
Q

List some factors that may potentiate warfarin?

A
  • Liver disease
  • P450 enzyme inhibitors e.g. amiodarone, ciprofloxacin
  • Cranberry juice
  • Drugs which displace warfarin from plasma albumin e.g. NSAIDs
  • Inhibit platelet function e.g. NSAIDs
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23
Q

Warfarin in pregnancy in breastfeeding - are they contraindicated, can they be used?

A

Breastfeeding - can be used
Pregnant - cannot be used - teratogenic

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24
Q

Side effects of warfarin?

A
  • Haemorrhage
  • Teratogenic, although can be used in breastfeeding mothers
  • Skin necrosis (due to thrombosis in venules)
  • Purple toes
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25
Q

In genital wart treatment what is used in the following situations?
1) Multiple, non-keratinised warts?
2) Solitary, keratinised wards?

A

1) Multiple, non-keratinised warts - topical podophyllum
2) Solitary, keratinised wards - cryotherapy

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26
Q

In which situation do you use topical podophyllum and in which do you use cryotherapy for the management of genital wards?

A

Multiple, non-keratinised warts - topical podophyllum
Solitary, keratinised wards - cryotherapy

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27
Q

Which strands of HPV cause genital warts?
What about cervical cancer?

A

1) 6&11 - genital warts
2) 16,18,33 - cervical cancer

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28
Q

Outline treatment options for salicylate overdose

A
  • Urinary alkalinisation with IV bicarbonate
  • Haemodialysis - if indicated with severe metabolic acidosis or pulmonary oedema
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29
Q

Reversal agent for benzodiazepines?

A

Flumazenil

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30
Q

What is the management of overdose with TCAs?

A

IV bicarbonate - reduces the risk of seizures and arrythmias in severe toxicity

Can consider lignocaine but priority is IV bicarb, and note to avoid 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.

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31
Q

True or false, dialysis is ineffective in management of TCA overdose?

A

True

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32
Q

What is the management of lithium overdose?

A
  • Mild-moderate toxicity - volume resuscitation with normal saline
  • Haemodialysis may be needed in severe toxicity
  • Sodium bicarb sometimes used
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33
Q

What are reversal agents for warfarin overdose?

A

Vit K, prothrombin complex

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34
Q

Reversal agent for heparin overdose?

A

Protamine sulphate

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35
Q

Management options for beta-blockers?

A
  • If bradycardic then atropine
  • In resistant cases, glucagon may be used
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36
Q

Management options for ethylene glycol poisoning?

A
  • Fomepizole, an inhibitor of alcohol dehydrogenase
  • Haemodialysis in refractory cases
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37
Q

What is the reversal agent used in treatment of poisoning with organophosphate insecticides?

A

Atropine

N.B the role of pralidoxime is unclear - meta-analyses failed to show any clear benefit

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38
Q

What is the reversal agent for digoxin toxicity?

A

Digoxin-specific antibody fragments

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39
Q

What is the reversal agent for iron poisoning?

A

Desferrioxamine, a chelating agent

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40
Q

What are the reversal agents for lead poisoning?

A

Dimercaprol, calcium edetate

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41
Q

What is the management for CO poisoning?

A

100% oxygen
Hyperbaric oxygen

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42
Q

What are the management options for cyanide poisoning?

A

Hydroxycobalamin
Any combination of amyl nitrate, sodium nitrite, and sodium thiosulfate

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43
Q

How to manage seasonal affective disorder (SAD)?

A

Treat the same way as depression
Begin with psychological therapies and follow up in 2 weeks to ensure no deterioration
Following this an SSRI can be given if needed

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44
Q

Which antibodies may be positive in idiopathic pulmonary fibrosis?

A

ANA in 30%, Rheumatoid factor in 10% - however the titres will be low

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45
Q

Outline the management of idiopathic pulmonary fibrosis

A
  • Pulmonary rehab
  • Supplementary oxygen
  • Eventually will require a lung transplant
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46
Q

Prognosis in idiopathic pulmmonary fibrosis?

A

Poor, average life expectancy is around 3-4 years

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47
Q

What will be the TLCO in idiopathic pulmonary fibrosis? Reduced or increased?

A

Reduced

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48
Q

Lung function test pattern in idiopathic pulmonary fibrosis?

A

FVC reduced < 70%
FEV1 reduced
FVC and FEV1 will be proportionately reduced so FEV1/FVC will be normal (sometimes slightly inreased)

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49
Q

Idiopathic pulmonary fibrosis in what age group commonly and more common in men or women?

A

50-70yrs
2x as commmon in men

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50
Q

Outline how skin prick tests are done

A

Drops of diluted allergen are placed on the skin after which the skin is pierced using a needle. A large number of allergens can be tested in one session. Normally includes a histamine (positive) and sterile water (negative) control. A wheal will typically develop if a patient has an allergy. Can be interpreted after 15 minutes

Useful for food allergies and also pollen

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51
Q

Skin prick tests are useful for what allergies?

A

Food allergies
Pollen

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52
Q

Which allergy tests useful for food allergies and pollen?

A

Skin prick test and RAST

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53
Q

Which allergy test useful for wasp / bee venom?

A

RAST

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54
Q

IgE RAST test determines the level of IgE to specific allergen or is it non-specific?

A

Specific

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55
Q

Outline how RAST tests are done

A

Determines the amount of IgE that reacts specifically with suspected or known allergens, for example IgE to egg protein. Results are given in grades from 0 (negative) to 6 (strongly positive)

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56
Q

Which allergy test is useful for contact dermatitis?

A

Skin patch testing

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57
Q

How soon are results from skin prick tests read?

A

After 15 minutes

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58
Q

How soon are results from skin patch testing read?

A

Read by a dermatologist after 48 hours

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59
Q

Give some risk factors for degenerative cervical myelopathy

A
  • Smoking
  • Genetics
  • Occupations - that expose patients to high axial loading
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60
Q

What is the gold standard investigation in suspected degenerative cervical myelopathy (DCM)?

A

MRI cervical spine

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61
Q

Features of DCM (degenerative cervical myelopathy)?

A
  • Pain (affecting the neck, upper or lower limb)
  • Loss of motor function (loss of digital dexterity, preventing simple tasks such as holding a fork or doing up their shirt buttons, arm or leg weakness/stiffness leading to impaired gait and imbalance)
  • Loss of sensory function causing numbness
  • Loss of autonomic function (urinary or faecal incontinence and/or impotence) - these can occur and do not necessarily suggest cauda equina syndrome in the absence of other hallmarks of that condition
  • Hoffman’s sign positive
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62
Q

What is Hoffman’s sign and in which condition is it positive?

A

Degenerative cervical myelopathy

Gently flicking one finger on a patient’s hand
Positive test results in reflex twitching of the other fingers on the same hand in response to the flick

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63
Q

How to manage suspected degenerative cervical myelopathy?

A

Urgent referral to specialist spinal services (neurosurgery or orthopaedic spinal surgery)

Decompressive surgery
Close observation for mild disease, but anything more progressive or severe requires surgery to prevent further deterioration
Physiotherapy should ONLY be initiated by specialist services, as manipulation can cause more spinal cord damage

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64
Q

Which drug is useful to manage tremor in drug-induced Parkinsonism?

A

Procyclidine

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65
Q

Which drug in Parkinson’s is associated with pulmonary fibrosis?

A

Cabergoline

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66
Q

Which medication in Parkinson’s management often has a reduced effectiveness with time?

A

Levodopa

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67
Q

Features of Rosacea?

A
  • Typically affects nose, cheeks and forehead
  • Flushing is often first symptom
  • Telangiectasia are common
  • Later develops into persistent erythema with - Papules and pustules
  • Rhinophyma
  • Ocular involvement: blepharitis
  • Sunlight may exacerbate symptoms
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68
Q

In rosacea, what are some simple measures that can be used - (i.e. not for specifc treatment of erythema / flushing or papules / pustules)?

A

Daily application of high-factor sunscreen
Camouflage creams may help reduce redness

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69
Q

How to manage predominant erythema / flushing in rosacea?

A

Topical brimonidine gel may be considered for patients with predominant flushing but limited telangiectasia

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70
Q

In rosacea, what can be considered for mild-to-moderate papules and / or pustules?

What about moderate to severe papules and / or pustules?

A

Topical ivermectin is first line
Alternatives: topical metro or topical azelaic acid

Combination of topical ivermectin + oral doxycycline

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71
Q

When to consider referral for rosacea?

A

When symptoms have not improved with optical management in primary care

Patients with rhinophyma

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72
Q

Predisposing factors for pityriasis versicolor?

A

Occurs in healthy individuals also
Immmunosuppression
Malnutrition
Cushing’s

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73
Q

What is the management for pityriasis versicolor, and what if it does not respond to this?

A

Ketoconazole shampoo

If not responding then send scrapings to confirm the diagnosis or consider alternative diagnoses and add oral itraconazole

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74
Q

Key feature that distinguishes scleritis from episcleritis?

A

Pain - pain in scleritis, not in episcleritis

Note scleritis is potentially sight threatening so more urgent

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75
Q

Risk factors for scleritis?

A
  • Rheumatoid arthritis: the most commonly
  • Associated condition
  • Systemic lupus erythematosus
  • Sarcoidosis
  • Granulomatosis with polyangiitis
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76
Q

Features of scleritis

A
  • Red eye
  • Painful
  • Watering and photophobia are common
  • Gradual decrease in vision
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77
Q

Outline management of scleritis

A
  • Same day assessment by an ophthalmologist
  • Oral NSAIDs typically used first line
  • Oral glucocorticoids may be used
  • Immunosuppressive drugs for resistant cases (and also to treat any underlying associated diseases)
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78
Q

Causes of dacytlitis?

A
  • Spondyloarthritis: e.g. Psoriatic and reactive arthritis
  • Sickle-cell disease
  • Other rare causes include tuberculosis, sarcoidosis and syphilis
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79
Q

In imaging in subarachnoid haemorrhage, which imaging is first line and then what other imaging can be done and why?

A

First-line = non-contrast CT head

Then can do CT angiography to identify the causal pathology and to plan definitive treatment

Then MRI angiography if CT angiography did not identify the cause of the subarachnoid haemorrhage

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80
Q

What to do if metformin is not tolerated due to GI side-effects?

A

Try a modified release formulation before switching to a second line agent

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81
Q

What is cataplexy?

A

Sudden and transient loss of muscular tone caused by strong emotion (e.g. laughter, being frightened). Features range from buckling knees to collapse

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82
Q

Around 2/3rds of patients with narcolepsy have ….

A

Around 2/3rds of patients with narcolepsy have cataplexy

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83
Q

How to differentiate between spider naevi and telangiectasia?

A

Spider naevi fill from the centre vs telangiectasia fills from the edge

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84
Q

Risk factors for spider naevi?

A
  • Liver disease
  • Pregnancy
  • COCP
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85
Q

Normal variants in ECGs for athletes?

A
  • Sinus bradycardia
  • 1st degree atrioventricular block
  • Wenckebach phenomenon (2nd degree - atrioventricular block Mobitz type 1)
  • Junctional escape rhythm
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86
Q

True or false, hydroceles can affect fertility?

A

False

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87
Q

Where are epididymal cysts found in relation to the testicle, and are they separate or attached to the body of the testicle?

A

Posterior to the testicle, separate from the body of the testicle

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88
Q

Give some conditions associated with epididymal cysts

A
  • Polycystic kidney disease
  • CF
  • VHL
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89
Q

What investigation is used to confirm the diagnosis of epididymal cysts?

A

Ultrasound

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90
Q

What is the management of epididymal cysts?

A
  • Usually supportive
  • Surgical removal or sclerotherapy may be attempted for larger or symptomatic cysts
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91
Q

What are the two types of hydroceles and what are they caused by?

A
  • Communicating: caused by patency of the processus vaginalis allowing peritoneal fluid to drain down into the scrotum. Communicating hydroceles are common in newborn males (clinically apparent in 5-10%) and usually resolve within the first few months of life
  • Non-communicating: caused by excessive fluid production within the tunica vaginalis
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92
Q

Give 3 things that hydroceles may develop secondary to?

A
  • Epididymo-orchitis
  • Testicular torsion
  • Testicular tumours
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93
Q

Describe the typical location of hydroceles in relation to the testicle and can you get above the mass or not on palpation?

A

Usually anterior to and below the testicle
You can get ‘above’ the mass on examination

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94
Q

Investigation for suspected hydrocele?

A

Clinical diagnosis, but ultrasound can be used if clinical uncertainty

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95
Q

At what point are hydroceles advised to be corrected in babies?

A

They usually self-resolve within 1 year of birth, however if they do not resolve spontaneously they are repaired

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96
Q

How are hydroceles managed in adults?

A

Conservative approach
Further investigation is usually warranted with ultrasound to exclude any underlying cause such as a tumour

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97
Q

True or false varicoceles are associated with infertility?

A

True

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98
Q

Varicoceles more common on right or left?

A

Left (>80%)

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99
Q

Investigation for varicoceles?

A

Doppler studies

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100
Q

Management for varicoceles?

A
  • Usually conservative
  • Occasionally surgery if patient is troubled by pain. Ongoing debate regarding the effectiveness of surgery to treat infertility
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101
Q

Outline the acute treatments for migraine/

A

First line: offer combo therapy with
- Oral triptan + NSAID or…
- Oral triptan + paracetamol

For young people 12-17 years consider a nasal triptan in preference to oral triptan

If above measures not effective or tolerated offer non-oral preparation of metoclopramide or prochlorperazine and consider adding a non-oral NSAID or triptan

Beware prescribing metoclopramide to young patients as acute dystonic reactions may develop

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102
Q

Which migraine prophylactic should be avoided in women of childbearing age?

A

Topiramate - it can be teratogenic and can reduce the effectiveness of hormonal contraceptives

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103
Q

What are the options for migraine prophylaxis?

A
  • Propranolol
  • Topiramate
  • Amitryptiline

If these fail advise a course of up to 10 sessions of acupuncture over 5-8 weeks
Advise riboflavin 400mg OD may help

For women with predictable menstrual migrain consider Frovatriptan 2.5mg BD or Zolmatriptan 2.5mg BD-TDS

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104
Q

Patient with AF and is haemodynamically unstable - what do you do?

A

Electrical cardioversion

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105
Q

Patient with new AF, haemodynamically stable. What to do if:
1) < 48 hrs from onset?
2) > 48 hrs from onset or uncertain (e.g. patient not sure when symptoms started)?

A

1) < 48 hrs - rate or rhythm control
2) > 48 hrs or uncertain - rate control
- If considered for long term rhythm control, delay cardioversion until they have been maintained on therapeutic anticoagultion for a minimum of 3 weeks

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106
Q

Rate controle should be offered as first line treatment strategy in AF except for (list some criteria)?

A
  • Atrial fibrillation has a reversible cause
  • Patients who have heart failure thought to be primarily caused by atrial fibrillation
  • New-onset atrial fibrillation (< 48 hours)
  • Atrial flutter whose condition is considered suitable for an ablation strategy to restore sinus rhythm
  • Those in whom rhythm-control strategy would be more suitable based on clinical judgement
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107
Q

3 rate control drugs / classes?

A
  • Beta-blockers
  • CCBs
  • Digoxin (only if very sedentary or other drugs ruled out because of comorbidities, may have a role in coexistent heart failure)
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108
Q

Which rhythm control agent is second line in patients following cardioversion?

A

Dronedarone

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109
Q

Which rhythm control agent is useful particularly in coexisting heart failure?

A

Amiodarone

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110
Q

Give 4 rhythm control agents?

A

Beta blockers
Dronedarone
Amiodarone
Flecainide

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111
Q

When is catheter ablation used in AF?

A

In those who have not responded to, or wish to avoid anti-arrythmic medication

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112
Q

How long should anticoagulation be used before and during / after catheter ablation?

A

4 weeks before and during the procedure, and needs afterwards based on chadvasc score

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113
Q

What to do about anticoagulation in patients undergoing catheter ablation after the procedure?

A

Still require anticoagulation based on the CHADVASC score

  • If = 0 - 2 months anticoagulation
  • If > 1 - long-term anticoagulation
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114
Q

Give 3 notable complications of catheter ablation for AF?

A
  • Cardiac tamponade
  • Stroke
  • Pulmonary vein stenosis
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115
Q

Definition of status epilepticus?

A
  • Single siezure lasting > 5 minutes or
  • > / = 2 seizures within a 5 minute period without the person returning to normal between them
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116
Q

Management of status epilepticus?

A
  • ABC
    Airway adjunct
    Oxygen
    Check blood glucose
  • In prehospital either buccal midazolam or rectal diazepam
  • In hospital IV lorazepam 4mg - then again after 5-10 minutes

If ongoing or established epilepticus - start second-line agent e.g. levetiracetam, phenytoin or sodium valproate

If no response within 45 minutes from onset - rapid induction of general anaesthesia or phenobarbital

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117
Q

Nail changes that can be seen in psoriasis / psoriatic arthropathy?

A
  • Pitting
  • Onycholysis (separation of the nail from the nail bed)
  • Subungual hyperkeratosis
  • Loss of the nail
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118
Q

Which medication is used to help prevent reaccumulation of ascites?

A

Spironolactone (aldosterone antagonist)

N.B. A loop diuretic may need to be added in non-responders

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119
Q

MOA of spironolactone and site of action?

A

Aldosterone antagonist - acts in the collecting ducts

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120
Q

Some indications for spironolactone?

A
  • Ascites: patients with cirrhosis develop a
  • Secondary hyperaldosteronism. Relatively large doses such as 100 or 200mg are often used
  • Hypertension: used in some patients as a NICE ‘step 4’ treatment
  • Heart failure
  • Nephrotic syndrome
  • Conn’s syndrome
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121
Q

Patient on 15mg Mirtazapine is complaining of sedation side effects, what can you do?

A

Increase the dose to 30mg ON
Mirtazapine is paradoxically, generally more sedating at lower BNF doses

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122
Q

2 side effects of mirtazapine that can actually be useful?

A

Sedation
Increased appetite

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123
Q

List some common causes of CKD

A
  • Diabetic nephropathy
  • Chronic glomerulonephritis
  • Chronic pyelonephritis
  • HTN
  • Adult PCKD
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124
Q

In rotator cuff injuries with the painful arc of abduction at what angles is it painful in subacromial impingement and in which angles is it painful for rotator cuff tears?

Also other features of rotator cuff injury - shoulder pain worse on …. and tenderness over what site?

A

Subacromial impingement - between 60 and 120 degrees
Rotator cuff tears - pain in first 60 degrees

Shoulder pain worse on abduction
Tenderness over anterior acromion

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125
Q

List different causes of rotator cuff injurt (different types)

A
  • Subacromial impingement
  • Calcific tendonitis
  • Rotator cuff tears
  • Rotator cuff arthropathy
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126
Q

List some conditions associated with vitiligo

A
  • T1DM
  • Addison’s disease
  • Autoimmune thyroid disorders
  • Pernicious anaemia
  • Alopecia areata
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127
Q

What is the Koebner phenomenon in relation to vitiligo?

A

Trauma may precipitate new lesions

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128
Q

Outline the management of Vitiligo

A
  • Sunblock for affected areas
  • Camouflage make-up
  • Topical corticosteroids may reverse the changes if applied early
  • Topical tacrolimus and phototherapy but careful with light-skinned patients
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129
Q

Jaundice within which time period after birth is always pathological?

A

Jaundice in the first 24 hours is always pathological and requires immediate paediatric assessment

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130
Q

List some causes of jaundice in the first 24 hours

A
  • Rhesus haemolytic disease
  • ABO haemolytic disease
  • Hereditary spherocytosis
  • G6PD
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131
Q

After what period in the post-natal period is jaundice considered prolonged?

A

After 14 days

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132
Q

Causes of neonatal jaundice from 2-14 days?

A
  • More red cells
  • More fragile red cells
  • Less developed liver function
  • Commonly in breastfed babies
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133
Q

What are the different investigations done in a prolonged jaundice screen in neonates (after 14 days)?

A
  • Conjugated and unconjugated bilirubin - note a raised conjugated bili could indicate biliary atresia which requires urgent surgical intervention
  • Direct antiglobulin test (Coomb’s test)
  • TFTs
  • FBC and blood film
  • Urine for MC&S and reducing sugars
  • U&Es and LFTs
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134
Q

List some causes of prolonged jaundice in the neonate (after 14 days)

A
  • Biliary atresia
  • Hypothyroidism
  • Galactosaemia
  • UTI
  • Breast milk jaundice
  • Prematurity
  • Congenital infections e.g. CMV, toxoplasmosis
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135
Q

When to start bone protection (bisphosphonate + calcium + vit D) in patients starting on long-term steroids?

A

Immediately, no need for DEXA or FRAX first

IF > 65 years or previously had fragility fracture
OR
IF < 65 years - offer bone density scan with further management dependent on

T-score > 0 - reassure
T-score between 0 - -1.5 - repeat bone density scan in 1-3 years
T-score < -1.5 - offer bone protection

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136
Q

List 3 most common cyanotic heart disease?

A
  • Tetralogy of fallot
  • Transposition of the great arteries
  • Tricuspid atresia
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137
Q

What is more common, transposition of the great arteries, or tetralogy of fallot?

A

Fallot’s is more common, however at birth TGA is more apparently common a patients generally present at around 1-2 months

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138
Q

List some of the most common causes of acynanotic congenital heart diseases?

A
  • VSD - most common - ~30%
  • ASD
  • PDA
  • Coarctation of the aorta
  • Aortic valve stenosis
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139
Q

Vitamin B6 overdose can lead to what?

A

Peripheral neuropathy

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140
Q

Where to insert nexplanon implant?

A

Subdermal, non-dominant arm

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141
Q

What is the first line treatment for Paget’s disease?

A

Bisphosphonates

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142
Q

Features of Paget’s disease?

A
  • Typically older males
  • Bone pain
  • Isolated raised ALP
  • Bone pain (e.g. pelvis, lumbar spine, femur)
  • Untreated features: bowing of tibia, bossing of skull
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143
Q

What happens with the serum calcium and phosphate in Paget’s disease?

A

Calcium and phosphate are typically normal

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144
Q

X-ray features in Paget’s disease?

A
  • Osteolysis in early diseaes - mixed lytic / sclerotic lesions later
  • Skull x-ray: thickened vault, osteoporosis circumscripta
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145
Q

Osteolysis in early diseaes - mixed lytic / sclerotic lesions later
Skull x-ray: thickened vault, osteoporosis circumscripta

Likely diagnosis?

A

Paget’s

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146
Q

What is seen in bone scintigraphy in Paget’s disease of the bone?

A

Increased uptake is seen focally at the sites of active bone lesions

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147
Q

What investigations done in Paget’s?

A

Bloods - raised ALP isolated, normal calcium and phosphate usually
X-rays - and skull x-rays
Bone scintigraphy

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148
Q

What is the management for Paget’s disease of the bone?

A

Bisphosphonate (either oral risedronate or IV zoledronate)

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149
Q

List some complications of Paget’s disease of the bone

A
  • Deafness (cranial nerve entrapment)
  • Bone sarcoma (1% if affected for > 10 years)
  • Fractures
  • Skull thickening
  • High-output cardiac failure
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150
Q

Features in malignant hyperthermia?

A

Raised end-tidal CO2
Raised temp - may appear diaphoretic, skin mottling

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151
Q

Which anaesthetic agents can cause malignant hyperthermia?

A

Volatile liquid anaesthetics - isoflurane, desflurane, sevoflurane

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152
Q

What is another adverse effect related to volatile liquid anaesthetics aside from risk of malignant hyperthermia?

A

Myocardial depression

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153
Q

What is a contra-indication for the use of nitrous oxide as an anaesthetic agent?

A

Pneumothorax
Since it may diffuse into gas-filled body compartments - increase in pressure

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154
Q

Key adverse effects related to propofol?

A
  • Hypotension
  • Pain on injection (due to activation of the pain receptor TRPA1)
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155
Q

Aside from its main use for induction / in already ventilated patients in intensive care, what is another beneficial property of propofol?

A

Has some anti-emetic effects - useful for patients with a high risk of post-operative vomiting

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156
Q

What is a key adverse effect of thiopental?

A

Laryngospasm

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157
Q

Adverse effects related to etomidate?

A
  • Primary adrenal suppression (secondary to reversibly inhibiting 11B- hydroxylase)
  • Myoclonus
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158
Q

Key adverse effects with ketamine?

A
  • Disorientation
  • Hallucinations
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159
Q

Why is ketamine useful as a rapid sequence induction agent in trauma situations?

A

Because it doesn’t cause a drop in BP

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160
Q

Clinical features in paraproteinaemias?

A
  • Hyperviscosity syndrome
  • Neuropathy (e.g. sensory, motor or autonomic dysfunction)
  • Renal dysfunction
  • Haematological abnormalities (e.g. anaemia, thrombocytopaenia, or leukopaenia)
  • Bone pain or pathologic fractures (in the context of multiple myeloma)
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161
Q

List the causes of benign and malignant paraproteinaemias

A

BENIGN:
- MGUS
- Transient paraproteinaemia (e.g. following an infection)

MALIGNANT:
- Multiple myeloma
- Waldenstrom’s macroglobulinaemia
- Primary amyloidosis (AL)
- B-cell lymphoproliferative disorders (e.g. CLL, NHL)

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162
Q

What are myxoid cysts?

A

Benign ganglion cysts usually found on the distal, dorsal aspect of the finger

There is usally osteoarthritis in the surrounding joint.

More common in middle-aged women

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163
Q

50 year old woman presents with swelling just proximal to the nail bed on the left great toe. She has a history of osteoarthritis but is usually well. What is the diagnosis?

A

Myxoid cyst

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164
Q

MS more common in men or women?

A

3x more common in women

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165
Q

What is the most common form of MS?

A

Relapsing-remitting

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166
Q

What is the pattern of disease in relapsing-remitting, primary progressive and secondary progressive forms of MS?

A

Relapsing-remitting: acute attacks (e.g. lasts 1-2 months) followed by periods of remission

Primary progressive: progressive deterioration from onset. More common in older people

Secondary progressive: relapsing-remitting patients who have deteriorated and have developed neurological signs and symptoms between relapses. Gait and bladder disorders are generally seen

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167
Q

In a patient on metformin, what HbA1C target should you aim for, and at what piont do you add a second drug?

A
  • Aim target HbA1C of 48 mmol/mol (6.5%)
  • Add second drug if HbA1C rises to 58mmol/mol (7.5%)
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168
Q

How often to check HbA1C targets in the type 2 diabetic?

A

HbA1C should be checked every 3-6 months until stable, then 6 monthly

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169
Q

What HbA1C target to set for patient on any drug which may cause hyperglycaemia (e.g. sulfonylurea) + lifestyle modification for management of T2DM?

A

53 mmol/mol (7.0%)

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170
Q

What are the thyroxine and TSH levels in sick euthyroid? Low or normal or high?

A

Often everything is low - TSH, thyroxine and T3

However mostly TSH is within normal range (inappropriately given the low thyroxine and T3)

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171
Q

How to manage sick euthyroid syndrome?

A

Changes are reversible upon recovery from the systemic illness and hence no treatment is usually needed - ask the GP to repeat TFTs in 6 weeks

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172
Q

Give 3 causes of optic neuritis

A
  • Multiple sclerosis - most common
  • Diabetes
  • Syphilis
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173
Q

Features of optic neuritis

A
  • Unilateral decrease in visual acuity over hours or days
  • Poor discrimination of colours, ‘red desaturation’
  • Pain worse on eye movement
  • Relative afferent pupillary defect
  • Central scotoma
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174
Q

What is the key investigation in optic neuritis?

A

MRI of the brain and orbits with gadolinium contrast

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175
Q

What is the management for optic neuritis?

A
  • High-dose steroids
  • Recovery usually takes 4-6 weeks
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176
Q

What is the 5 year risk of developing multiple sclerosis in optic neuritis?

A

MRI - if > 3 white matter lesions, 5 year risk of developing MS is ~50%

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177
Q

What is the guidance for the units of alcohol to drink per week?

A

No more than 14 units of alcohol per week. If you do drink as much as 14 units per week, spread this evenly over 3 days or more

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178
Q

Management of blepharitis?

A
  • Softening of the lid margin using hot compresses twice a day
  • Lid hygiene - mechanical removal of debris from lid margins
  • Artificial tears for symptom relief in people with dry eyes or an abnormal tear film
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179
Q

What may occur secondary to blepharitis?

A

Secondary conjunctivitis

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180
Q

Blepharitis may be either due to …. or …. / ….
Blepharitis is also more common in patients with …..

A

Blepharitis may be either due to meibomian gland dysfunction (common, posterior blepharitis) or seborrheic dermatitis / staphylococcal infection (less common, anterior blepharitis)

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181
Q

Anterior uveitis is associated with which HLA?

A

HLA-B27

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182
Q

Give some conditions associated with anterior uveitis

A
  • Ankylosing spondylitis
  • Reactive arthritis
  • UC, Crohn’s
  • Behcet’s
  • Sarcoidosis - bilateral disease may be seen
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183
Q

Outline the management of anterior uveitis

A
  • Urgent review by ophthalmology
  • Cycloplegics e.g. atropine, cyclopentolate (dilates the pupil which helps relieve pain and photophobia)
  • Steroid eye drops
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184
Q

Features of anterior uveitis?

A
  • Acute onset
  • Ocular discomfort and pain
  • Pupil may be small +/- irregular due to sphinchter muscle contraction
  • Photophobia (often intense)
  • Blurred vision
  • Red eye
  • Lacrimation
  • Ciliary flush - a ring of red spreading outwards
  • Hypopon - pus and inflammatory cells in the anterior chamber, often resulting in a visible fluid level
  • Visual acuity initially normal - impaired
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185
Q

List some neurological sequelae of meningitis

A
  • Sensorineural hearing loss (most common)
  • Seizures
  • Focal neurological deficit
  • Infective - sepsis, intracerebral abscess
  • Pressure - brain herniation, hydrocephalus
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186
Q

Aside from neurological sequelae, name an endocrine complication of meningitis?

A

Waterhouse-Friderichsen syndrome (adrenal insufficiency secondary to adrenal haemorrhage)

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187
Q

How long does acute pericarditis usually last?

A

4-6 weeks

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188
Q

List some causes of acute pericarditis?

A
  • Viral infections (Coxsackie)
  • TB
  • Uraemia
  • Post-MI
  • RT
  • Connective tissue disease - SLE, RhA
  • Hypothyroidism
  • Malignancy - lung cancer, breast cancer
  • Trauma
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189
Q

What is the nature of the chest pain in acute pericarditis, and relieved on what position?

A

Pleuritic
Often relieved on sitting forwards

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190
Q

Clinical features of acute pericarditis?

A
  • Chest pain - pleuritic, often relieved on sitting forwards
  • Pericardial rub
  • Non-productive cough, dyspnoea, flu-like symptoms
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191
Q

What is the most specific ECG marker for pericarditis?

A

PR depression

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192
Q

ECG features in acute pericarditis?

A
  • Global / widespread ST elevation (not limited to territories)
  • ‘Saddle shaped’ ST elevation
  • PR depression
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193
Q

What investigations in acute pericarditis?

A

ECG
Bloods and trops
TTE

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194
Q

High risk features that warrant inpatient rather than outpatient management of acute pericarditis?

A
  • Fever > 38C
  • Elevated troponin
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195
Q

Management of acute pericarditis?

A

Depends on the cause e.g. if viral - often nothing

Often managed as outpatient

Avoid strenuous physical activity until symptom resolution and normalisation of inflammatory markers

NSAIDs + colchicine for acute idiopathic or viral pericarditis
- until symptom resolution and normalisation of inflammatory markers (usually 1-2 weeks) followed by tapering of dose

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196
Q

What is the recommended antibiotic and duration of therapy for lower UTI in non-pregnant women?

A

Trimethoprim or nitrofurantoin for 3 days

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197
Q

When to send a urine culture in lower UTIs?

A
  • > 65 years
  • Visible or non-visible haematuria
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198
Q

True or false - you need to treat asymptomatic bacteriuria in pregnant women?

A

True - due to significant risk of progression to acute pyelonephritis

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199
Q

How to manage symptomatic UTI in pregnant women?

A
  • Urine culture always send
  • Abx - nitro (should be avoided near term)
    second line is amox of cefalexin
  • Note trimethoprim is teratogenic in the first trimester and should be avoided during pregnancy
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200
Q

How to manage asymptomatic bacteruria in pregnant women?

A
  • Urine culture should be performed routinely at the first antenatal visit
  • Immediate antibiotic prescription (nitro - but avoid near term), amox or cefalexin - 7 day course
  • Do another culture following completion of treatment as a test of cure
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201
Q

How to treat lower UTI in men?

A

Trimethoprim or nitrofurantoin for 7 days

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202
Q

How to treat UTI in catheterised patients?

A
  • Do NOT treat asymptomatic bacteruria in catheterised patients
  • If the patient is symptomatic they should be treated with 7 day antibiotic course
  • Remover or change the catheter ASAP if has been in place > 7 days
203
Q

How to treat acute pyelonephritis?

A

IV fluids, abx - usually broad spectrum cephalosporin or a quinolone (for non-pregnant women) for 10-14 days

204
Q

List some key indications for NIV

A
  • COPD with resp acidosis 7.25-7.35
  • T2RF secondary to chest wall deformity, neuromuscular disease or OSA
  • Cardiogenic pulmonary oedema unresponsive to CPAP
  • Weaning from tracheal intubation
205
Q

Recommended initial settings for BIPAP in COPD:
1) EPAP
2) IPAP
3) Back up rate
4) Back up I:E ratio

A

1) 4-5cm H2O
2) IPAP 10cm H2O or 12-15cm H2O
3) Back up rate: 15 breaths per minute
4) Back up I:E ratio : 1:3

206
Q

How soon before urea breath test should antibacterials or antisecretory drug e.g. PPI?

A

Should not do urea breath test within 4 weeks of treatment with antibacterial or within 2 weeks of an antisecretory drug e.g. PPI

207
Q

Which investigation can be used to test for H pylori eradication?

A

Urea breath test

208
Q

List some investigations done in suspected H.Pylori infection?

A

Urea breath test
Rapid urease test e.g. CLO test
Serum antibody
Culture of gastric biopsy
Gastric biopsy
Stool antigen test

209
Q

What can be seen on the blood film in multiple myeloma?

A

Rouleaux formation

210
Q

After how long after a stroke can we consider safe initiation of anticoagulation therapy (e.g. apixaban)

A

2 weeks

211
Q

What to replace ACEis with in people with ACEi related cough?

A

ARBs

212
Q

List some exacerbating factors for psoriasis

A
  • Trauma
  • Alcohol
  • Drugs e.g. beta-blockers, lithium, anti-malarials (chloroquine and hydroxychloroquine), NSAIDs and ACEis, infliximab
  • Withdrawal of systemic steroids
213
Q

Aside from antibiotics such as clindamycin or third generation cephalosporins, what other drug is a risk factor for c.diff?

A

PPIs

214
Q

What is the transmission route for c.diff?

A

Faeco-oral via ingestion of spores

215
Q

Severe c.diff can lead to?

A

Toxic megacolon

216
Q

How to classify mild, moderate, severe and life threatenning c.diff?

A

Mild - normal WCC
Moderate - Raised WCC ( < 15 x 10^9/L), typically 3-5 loose stools per day
Severe - Raised WCC or an acutely raised creatinine (>50% above baseline), temp > 38.5, evidence of colitis (abdo or radiological signs)
Life threatening - hypotension, partial or complete ileus, toxic megacolon, CT evidence of severe disease

217
Q

True or false - c.diff antigen positivity means there is active infection?

A

False - only shows exposure to the bacteria, rather than current infection

218
Q

What is first, second and third line treatment for c.diff?

A
  1. First line - oral vancomycin 10 days
  2. Second line - oral fidaxomicin
  3. Third-line - oral vancomycin +/- IV metronidazole
    Consider specialist advice for consideration of surgery in life-threatening cases
219
Q

How to manage recurrent episode of c.diff?

A

If within 12 weeks of symptom resolution - oral fidaxomicin
If after 12 weeks of symptom resolution - oral vancomycin or fidaxomycin

Faetal microbiota transplant

220
Q

What are the isolation precautions for c.diff?

A

Isolation in side room - until there has been no diarrhoea (types 5-7 on the bristol stool chart) for at least 48 hours

Gloves and apron, handwashing

221
Q

List some sickle-cell crises

A
  • Thrombotic, ‘vaso-occlusive’, ‘painful crises’
  • Acute chest syndrome
  • Anaemic - aplastic, sequestration
  • Infection
222
Q

What can precipitate thrombotic crises in sickle cell?

A

Infection, dehydration, deoxygenation (high altitude)

223
Q

Where can infarcts occur in thrombotic crises in sickle cell?

A

Various areas
Bones e.g. avascular necrosis of the hip
Hand-foot syndrome in children
Lungs, spleen, brain

224
Q

Features of acute chest syndrome in sickle cell disease?

A

Dyspnoea, chest pain, pulmonary infiltrates on CXR, low pO2

225
Q

What is the classic feature of acute chest syndrome on CXR in sickle cell disease?

A

Infiltrates

226
Q

What is the most common cause of death after childhood in sickle cell disease?

A

Acute chest syndrome

227
Q

Outline management for acute chest syndrome

A
  • Pain relief
  • Respiratory support e.g. oxygen therapy
  • Antibiotics - infection may precipitate acute chest syndrome, and findings often hard to differentiate from it
228
Q

Aplastic crisis is precipitate by what in sickle cell disease?

A

Infection with parvovirus

229
Q

Feature in aplastic crises in sickle cell disease

A
  • Sudden fall in haemoglobin
  • Bone marrow suppression - reduced reticulocyte count
230
Q

Features of sequestration crisis in sickle cell disease?

A
  • Worsening of anaemia
  • Increased reticulocyte count
231
Q

What is a key difference between aplastic crises and sequestration crises?

A

Reduced reticulocyte count in aplastic crises vs increased reticulocyte count in sequestration crises

232
Q

How does the TIBC differ in iron deficinecy anaemia versus anaemia of chronic disease?

A

Raised in IDA vs not in anaemia of chronic disease

233
Q

What is a useful measure to differentiate between IDA and anaemia of chronic disease in iron studies?

A

TIBC - will be raised in IDA, not in anaemia of chronic disease

234
Q

What can raise the TIBC?

A
  • IDA
  • Pregnancy
  • Oestrogen
235
Q

How to calculate the transferrin saturation?

A

Serum iron / TIBC

236
Q

When will ferritin be raised?

A

Inflammation

237
Q

When will ferritin be low?

A

IDA

238
Q

What will happen to the ferritin and TIBC in anaemia of chronic disease?

A

Ferritin will be normal or raised
TIBC will be reduced

239
Q

How to calculate the anion gap, and what is a normal range for the anion gap, in mmol/L?

A

Anion gap = (Na + K) - (HCO3- + Cl-)

8-14 mmol/L

240
Q

List causes of a raised anion gap metabolic acidosis

A
  • Lactate - shock, hypoxia
  • Ketones - diabetic ketoacidosis, alcohol
  • Urate - renal failure
  • Acid poisoning - salicylates, methanol
  • 5-oxoproline: chronic paracetamol use
241
Q

List causes of a normal anion gap or hyperchloraemic metabolic acidosis

A
  • GI bicarb loss: diarrhoea, uterosigmoidostomy, fistula
  • RTA
  • Drugs e.g. acetazolamide
  • Ammonium chloride injection
  • Addison’s disease
242
Q

Classical triad in renal cell carcinoma?

A
  • Haematuria
  • Loin pain
  • Abdominal pain
243
Q

Features of renal cell carcinoma?

A
  • Classical triad - haematuria, loin pain, abdominal mass
  • Pyrexia of unknown origin
  • Left varicocele (due to occlusion of left testicular vein)
  • Endocrine effects: secrete EPO (polycythaemia), parathyroid hormone (hypercalcaemia), renin, ACTH
  • 25% have metastases at presentation
244
Q

Which type of urological cancer can cause varicoceles?

A

Renal cell carcinoma - due to occlusion of left testicular vein

245
Q

Endocrine effects that can occur in renal cell carcinoma?

A
  • EPO secretion - polycythaemia
  • Parathyroid hormone - hypercalcaemia
  • Renin
  • ACTH
246
Q

Features of chlamydia in women?
In men?

A

Asymptomatic in 70% of women, 50% of men

1) Women - cervicitis (discharge, bleeding), dysuria
2) Men - urethral discharge, dysuria

247
Q

Give some transient or spurious causes of non-visible haematuria?

A
  • UTI
  • Menstruation
  • Vigorous exercise
  • Sexual intercourse
248
Q

List some causes of persistent non-visible haematuria?

A
  • Cancer (bladder, renal, prostate)
  • Stones
  • BPH
  • Prostatitis
  • Urethritis e.g. chlamydia
  • Renal causes e.g. IgA nephropathy, thin basement membrane disease
249
Q

Give some spurious causes of visible haematuria but negative on dipstick - i.e. urine appears red / orange but no evidence of blood on dipstick

A
  • Foods - beetroot, rhubarb
  • Drugs - rifampicin, doxorubicin
250
Q

What are the guidelines for 2 week wait referral for haematuria?

A

Aged > = 45 years AND
- Unexplained visible haematuria without UTI or
- Visible haematuria that persists or recurs after successful treatment of UTI

  • Age > = 60 years AND have unexplained nonvisible haematuria and either dysuria or a raised WCC on a blood test
251
Q

What are the criteria for non-urgent referral for haematuria?

A

Aged > = 60 with reucrrent or persistent unexplained UTI

Note patients under 40 with normal renal function, no proteinuria and who are normotensive, do not need to be referred and may be managed in primary care

252
Q

BNP is produced by what part of the heart in response to strain?

A

Left ventricular myocardium

253
Q

Give one thing that can cause a falsely raised BNP (not heart pathology)?

A

Reduced excretion in CKD

254
Q

True or false, BNP can be used as a marker of prognosis in patients with chronic heart failure, and as a treatment marker (i.e. effective treatment lowers BNP)?

A

True

255
Q

True or false, ACEi’s and beta-blockers reduce mortality in heart failure with preserved ejection fraction?

A

False

256
Q

What is the first line treatment for chronic heart failure?

A

ACEi and beta- blocker
But not at the same time - one then the other

Beta blockers licenced include: bisoprolol, carvedilol, nebivolol

257
Q

What is second line therapy in chronic heart failure?

A

Aldosterone antagonists

SGLT-2 inhibitors

258
Q

What is third line therapy for chronic heart failure?

A
  • Ivabradine - if sinus rhythm < 75bpm, LVEF < 35%
  • Salcubitril-valsartan - LVEF < 35%, HFrEF who are symptomatic on ACEi’s or ARBs. Should be initiated following ACEi or ARB wash-out period
  • Digoxin - inotropic, strongly indicated if there is AF
  • Hydralazine + nitrate - especially in Afro-Caribbean patients
  • Cardiac resynchronisation therapy - widened QRS e.g. LBBB on ECG
259
Q

What vaccines do people with chronic heart failure need?

A
  • Offer annual influenza vaccine
  • One off pneumococcal vaccine

Adults usually require just one dose but those with asplenia, splenic dysfunction or chronic kidney disease need a booster every 5 years

260
Q

What is the most common type of oesophageal cancer, and is more likely to develop in those with a history of GORD or Barret’s?

A

Adenocarcinoma

261
Q

What is the most common type of oesophageal cancer in the developing world?

A

Squamous cell cancer

262
Q

Where are adenocarcinomas located along the oesophagus?

A

Lower third - near the gastroesophageal junction

263
Q

Where are squamous cell carcinomas located along the oesophagus?

A

Upper two thirds of the oesophagus

264
Q

List some risk factors for adenocarcinoma of oesophagus

A
  • GORD
  • Barret’s oesophagus
  • Smoking
  • Obesity
265
Q

List some risk factors for squamous cell cancer of oesophagus

A
  • Smoking
  • Alcohol
  • Achalasia
  • Plummer-Vinson syndrome
  • Nitrosamine rich diet
266
Q

In suspected oesophageal cancer, which investigations are used for the following?

1) Diagnosis?
2) Locoregional staging?
3) Initial staging?
4) To detect occult metastases if not seen on initial staging scans?
5) To detect occult peritoneal disease?

A

1) Diagnosis = OGD
2) Locoregional staging = Endoscopic u/s
3) Initial staging = CT CAP
4) To detect occult metastases if not seen on initial staging scans = FDG-PET-CT
5) To detect occult peritoneal disease = Laparoscopy

267
Q

What is the treatment for oesophageal cancer?

A

Operable disease (T1N0M0) - surgical resectin - most commonly Ivor-Lewis type oesophagectomy
- N.B risk of anastamotic leak - with intrathoracic anastamosis resulting in mediastinitis

Adjuvant chemo

268
Q

What is the inheritance pattern of sickle cell disease?

A

Autosomal recessive

269
Q

At what age do sickle cell homozygotes tend to develop symptoms, and why?

A

4-6 months - because abnormal HbSS molecules take over from fetal haemoglobin

270
Q

What is the definitive investigation for sickle cell disease?

A

Haemoglobin electrophoresis

271
Q

Verapamil or CCBs are contraindicated in which type of arrythmia?

A

Ventricular tachycardia

272
Q

What is the appropriate medical management for ventricular tachycardia?

Non medical?

A
  • Amiodarone - ideally through a central line
  • Lidocaine - use with caution in severe LV impairment
  • Procainamide

Note if drug therapy fails
- Electrophysiological study (EPS)
- Implantable cardioverter-defibrillator - especilly in patients with significantly impaired LV function

NOTE: If SBP < 90mmHg, chest pain, heart failure, syncope - IMMEDIATE CARDIOVERSION

273
Q

A 65-year-old man is discharged from hospital following a thrombolysed ST-elevation myocardial infarction. Other than a history of depression he has no past medical history of note. Examination of his cardiorespiratory system today was normal. His stay on the coronary care unit was complicated by the development of dyspnoea and an echo show a reduced left ventricular ejection fraction. Other than standard treatment with an ACE inhibitor, beta-blocker, aspirin, clopidogrel and statin, what other type of drug should he be taking?

A

Aldosterone antagonist as the patient has reduced LVEF.
Note: a loop diuretic is not indicated unless there is evidence of fluid overload

274
Q

Describe how to manage the oxygen therapy for a patient with COPD?

A
  • Acutely ill patients - high flow oxygen at 15/L min
  • At risk of hyercapnia (retainers) who are stable - 88-92% target
  • Unwell with COPD prior to availability of blood gases, use a 28% venturi mask at 4 L / min and aim for O2 sats of 88-92% for patients with risk factors for hypercapnia byt no prior history of respiratory acidosis
  • Adjust the target range to 94-98% if the PCO2 is normal
275
Q

What is torsades de pointes?

A

Torsades de pointes is a form of polymorphic ventricular tachycardia associated with a long QT interval

276
Q

How can Torsades de pointes lead to death?

A

Torsades de pointes is a polymorphic ventricular tachycardia associated with a long QT interval. It may deteriorate into VF and hence lead to sudden death

277
Q

What is the definitive treatment for Torsades de pointes?

A

IV Magnesium Sulphate

278
Q

List causes of Torsades de pointes

A
  • Congenital - Jervell-Lange-Nielsen Syndrome, Romano-Ward syndrome
  • Antiarrythmics: amiodarone, sotalol, class 1a antiarrythmic drugs
  • Tricyclic antidepressants
  • Antipsychotics
  • Chloroquine
  • Terfenadine
  • Erythromycin
  • Electrolyte - hypocalcaemia, hypokalaemia, hypomagnesaemia
  • Myocarditis
  • Hypothermia
  • Subarachnoid haemorrhage
279
Q

Outline the medical management in Alzheimer’s

A
  • Acetylcholinesterase inhibitors (donepezil, galantamine and rivastigmine) - for mild-moderate disease
  • NMDA receptor antagonist (memantine) - either for severe disease, as add-on therapy or if acetylcholinesterase inhibitors are contra-indicated
  • Antipsychotics only if patients at risk of harming themselves or others, or when the agitation, hallucinations or delusions are causing them severe distress
280
Q

When is Donepezil contra-indicated?

A

In patients with bradycardia

281
Q

Common adverse effect with Donepezil?

A

Insomnia

282
Q

What is the most common cause of nephrotic syndrome in children?

A

Minimal change disease
(75% in children, 25% in adults)

283
Q

Give some causes of minimal change syndrome?

A

Mostly idiopathic, but in 10-20% a cause can be found e.g. :
- Drugs e.g. NSAIDs, Rifampicin
- Hodgkin’s lymphoma, Thymoma
- Infectious mononucleosis

284
Q

Outline the features of minimal change syndrome

A
  • Nephrotic syndrome
  • Normotension - hypertension is rare
  • Highly selective proteinuria - intermediate sized proteins such as albumin and transferrin leak through the glomerulus
  • Renal biopsy features - normal glomeruli on light microscopy, EM - fusion of podocytes and effacement of foot processes
285
Q

What is the prognosis in miimal change syndrome? - tip remember the rule of thirds

A

1/3 have just one episode
1/3 have infrequent relapses
1/3 have frequent relapses which stop just before adulthood

286
Q

Outline the management for minimal change disease

A
  • Oral corticosteroids - 80% are steroid-responsive
  • Cyclophosphamide for non-steroid responsive cases
287
Q

What test is best used to assess for acute liver failure?

A

Prothrombin time

LFTs do not always accurately reflect the synthetic function of the liver. This is best assessed by looking at the PT and the albumin level

PT has a shorter half-life than albumin, making it a better measure of acute liver failure than albumin

288
Q

List some causes of acute liver failure

A
  • Paracetamol overdose
  • Alcohol
  • Viral hepatitis (usually A or B)
  • Acute fatty liver of pregnancy
289
Q

What are the features of acute liver failure?

A
  • Jaundice
  • Coagulopathy - raised PT
  • Hypoalbuminaemia
  • Hepatic encephalopathy
  • Renal failure - ‘hepatorenal syndrome’
290
Q

Which blood group is associated with higher risk of gastric cancer, and which associated with a higher risk of duodenal cancer?

A

Blood group A - higher risk of gastric cancer
Blood group O - higher risk of duodenal cancer

291
Q

Features of hypocalcaemia?

A
  • Tetany - muscle twitching, cramping and spasm
  • Perioral paraesthesia
  • If chronic - depression, cataracts
  • ECG: prolonged QT interval
  • Trousseau’s sign
  • Chvostek’s sign
292
Q

Which anti-hypertensive useful in diabetics?

A

ACEi’s e.g. Ramipril

293
Q

List drugs which cause a hepatocellular drug induced liver injury picture

A
  • Paracetamol
  • Sodium valproate, phenytoin
  • MAOIs
  • Halothane
  • Anti-TB - Rifampicin, Isoniazid, Pyrazinamide
  • Statins
  • Alcohol
  • Amiodarone
  • Methyldopa
  • Nitrofurantoin
294
Q

List drugs that tend to cause cholestasis (+/- hepatitis)

A
  • COCP
  • Antibiotics - flucloxacillin, co-amox, erythromycin
  • Anabolic steroids, testosterones
  • Phenothiazines: chlorpromazine, prochlorperazine
  • Sulphonylureas
  • Fibrates
  • Rare - nifedipine
295
Q

Give 3 medications that can cause liver cirrhosis

A
  • Methotrexate
  • Methyldopa
  • Amiodarone
296
Q

What is the initial phase and continuation phase of TB therapy - which medications and what duration of therapy?

What about for latent TB

What about for meningeal TB

What is directly observed therapy and in whom is it useful?

A

INITIAL PHASE - for first 2 months:
- Rifampicin
- Isoniazid
- Pyrazinamide
- Ethambutol

CONTINUATION PHASE - for the next 4 months:
- Rifampicin
- Isoniazid

LATENT TB - 3 months of Isoniazid + Pyridoxine (not pyrazinamide) + Rifampicin OR 6 months of Isoniazid + Pyridoxine (not pyrazinamide)

MENINGEAL TB - prolonged period (at least 12 months) with addition of steroids

DIRECTLY OBSERVED THERAPY - 3x a week dosing regimen in:
- Homeless people with active TB
- Patients likely to have poor concordance
- All prisoners with active or latent TB

297
Q

What is immune reconstitution disease in TB?

A

A complication that occurs typically 3-6 weeks after starting treatment for TB that often presents with enlarging lymph nodes

298
Q

Adverse effects associated with rifampicin?

A
  • Potent liver enzyme inducer
  • Hepatitis
  • Orange secretions
  • Flu-like symptoms
299
Q

What is given alongside isoniazid to help prevent peripheral neuropathy?

A

Pyridoxine (Vitamin B6)

300
Q

Adverse effects associated with isoniazid?

A
  • Peripheral neuropathy - prevented with pyridoxine (vitamin B6)
  • Hepatitis
  • Agranulocytosis
  • Liver enzyme inhibitor
301
Q

Adverse effects associated with pyrazinamide?

A
  • Hyperuricaemia causing gout
  • Arthralgia
  • Myalgia
  • Hepatitis
302
Q

Key adverse effect associated with ethambutol?

A
  • Optic neuritis - therefore check visual acuity before and during treatment
303
Q

In animal bites - often dogs and cats, what is the most common isolated organism?

A

Pasteurella multocida

304
Q

How to manage animal bites?

Which antibiotic is best, and then what if allergic?

A
  • Clean wound
  • Pucnture wounds should not be sutured closed unless cosmesis is at risk
  • Abx: Co-amoxiclav
  • If penicillin allergic: doxycycline + metronidazole
305
Q

What is the treatment for human bites?

A

Co-amoxiclav, as for animal bites

The risk for viral infections e.g. HIV and Hep C should also be considered

306
Q

In whom should adenosine be avoided?

A

Asthmatics due to bronchospasm

307
Q

Adverse effects with adenosine?

A
  • Chest pain
  • Bronchospasm
  • Transient flushing
  • Can enhance conduction down accessory pathways, resulting in increased ventricular rate (e.g. WPW syndrome)
308
Q

How to administer adenosine - large or small cannula?

A

Large calibre cannula due to its short half-life

309
Q

Over 80% of pancreatic tumours are ….. which typically occur at the …. of the pancreas

A

Over 80% of pancreatic tumours are adenocarcinomas which typically occur at the head of the pancreas

310
Q

List some associations for pancreatic cancer

A
  • Increasing age
  • Smoking
  • Diabetes
  • Chronic pancreatitis
  • HNPCC
  • MEN
  • BRCA2 gene
  • KRAS mutation
311
Q

What is Courvoisier’s law?

A

In the presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to gallstones

312
Q

What is the most common histological subtype in pancreatic cancer?

A

Adenocarcinomas

313
Q

Features of pancreatic cancer?

A
  • Painless jaundice, may have palpable gallbladder (Courvoisier’s sign)
  • Pale stools, dark urine, pruritis
  • Cholestatic LFTs
  • Abdominal masses - hepatomegaly (due to mets), gallbladder, epigastric mass (from the primary tumour)
  • Loss of exocrine function - e.g. steatorrhea
  • Loss of endocrine function - e.g. DM
  • Atypical back pain
  • Migratory thrombophlebitis (Trousseau’s sign) more commonly than in other cancers
  • Anorexia, weight loss, epigastric pain
313
Q

What is the most common site on the pancreas where pancreatic (adeno-)carcinomas occur?

A

Head of the pancreas

314
Q

What is the key investigation in suspected pancreatic cancer?

A

HRCT
Note: imaging may demonstrate the double duct sign - presence of simultaneous dilatation of the common bile and pancreatic ducts

315
Q

What is the surgical management for pancreatic cancer?

A

Whipple’s resection (pancreaticoduodonectomy) - for resectable lesions at the head of the pancreas

Adjuvant chemo is usually given following the surgery

316
Q

What are 2 key side effects in Whipple’s disease?

A
  • Dumping syndrome
  • PUD
317
Q

What is often done for palliative management in pancreatic cancer?

A

ERCP with stenting

318
Q

List some adverse effects associated with PPIs

A
  • Hyponatraemia, hypomagnasaemia
  • Osteoporosis - increased risk of fractures
  • Microscopic colitis
  • Increased risk of c.diff infections
319
Q

What organism is predominant in Bacterial Vaginosis?

A

Gardnerella Vaginalis

320
Q

How does BV affect vaginal pH?

A

Increases it - because the Gardnerella Vaginalis leads to a consequent fall in lactic acid producing aerobic lactobacilli resulting in a raised vaginal pH

321
Q

What are Ansel’s criteria for BV?

A

3 of the 4 points should be present:
- Thin, white, homogenous discharge
- Clue cells on microscopy: stippled vaginal epithelial cells
- Vaginal pH > 4.5
- Positive whiff test (addition of potassium hydroxide results in a fishy odour)

322
Q

What is the management of bacterial vaginosis?

A
  • If incidental asymptomatic - no treatment (unless undergoing termination of pregnancy)
  • If symptomatic - oral metro for 5-7 days (note a single dose of metro 2g may be used if adherence may be an issue). Topical metro or clindamycin as alternatives
  • If pregnant asymptomatic - speak to the obstetrician
  • If pregnant symptomatic - oral metro - but not the higher stat dose of 2g
323
Q

Conditions associated with coeliac’s disease?

A

Dermatitis herpetiformis
Autoimmune disorders - T1DM and autoimmune hepatitis

324
Q

What is the key serology done in investigation of Coeliac disease?

A
  • Tissue Transglutaminase TTG antibodies (IgA) is first choice
  • Enomyseal antibody (IgA)
325
Q

What is the gold standard investigation in Coeliac disease?

A

Endoscopic intestinal biopsy - often from the duodenum

Features:
- Villous atrophy
- Crypt hyperplasia
- Increase in intraepithelial lymphocytes
- Lamina propria infiltration with lymphocytes

326
Q

What are the 4 phases in subacute (De Quervain’s thyroiditis?

A
  1. Phase 1 (lasts 3-6 weeks) - hyperthyroidism, painful goitre, raised ESR
  2. Phase 2 (1-3 weeks) - euthyroid
  3. Phase 3 (weeks-months) - hypothyroidism
  4. Phase 4: thyroid structure and function goes back to normal
327
Q

What is the key investigation in suspected subacute (De Quervain’s) thyroiditis and what will it show?

A

Thyroid scintigraphy - globally reduced uptake of iodine-131

328
Q

What is the management of subacute (De Quervain’s) thyeroiditis?

A
  • Usually self-limiting - most patients do not require treatment
  • Thyroid pain may respond to aspirin or other NSAIDs
  • In more severe cases, steroids are used, particularly if hypothyroidism develops
329
Q

What will thyroid scintigraphy show in subacute (De Quervain’s) thyroiditis?

A

Globally reduced uptake of iodine-131

330
Q

What is the inheritance pattern in Huntington’s disease, and what is the mechanism, and which chromosome is it on?

A
  • Autosomal dominant
  • Trinucleotide repeat disorder - repeat expansion of CAG - phenomenon of anticipation occurs where the disease presents at an earlier age in successive generations
  • Due to defect in hintingtin gene on chromosome 4
331
Q

Features of Huntington’s disease?

A
  • Chorea
  • Personality changes (e.g. irritability, apathy, depression) and intellectual impairment
  • Dystonia
  • Saccadic eye movements
332
Q

What is the mechanism of action of statins?

A

Inhibit the action of HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis

333
Q

Give 3 absolute contraindications for statins, and one other relative contraindication?

A

Absolute:
- Macrolides e.g. erythromycin, clarithromycin - important interaction
- Pregnancy
- Liver impairment with serum transaminase 3x the upper limit of the referance range

Relative:
- History of intracerebral haemorrhage - some evidence that it may increase risk of ICH in people with history of stroke

334
Q

Give 3 adverse effects linked to statins?

A
  • Myopathy - including myalgia, myositis, rhabdomyolysis and asymptomatic raised CK
  • Liver impairment
  • May increase the risk of intracerebral haemorrhage in patients who’ve previously had stroke
335
Q

Risk factors for myopathy in statin use?
Which type of statins more commonly cause myopathy and which less commmonly?

A

Risk factors:
- Age
- Females
- Low BMI
- Presence of multisystem disease e.g. diabetes

More common in lipophilic statins (simvastatin, atorvastatin) than relatively hydrophilic statins (rosuvastatin, pravastatin, fluvastatin)

336
Q

True or false, everyone with type 2 diabetes mellitus must be on statins?

A

False - they should now be assessed using QRISK 2 like any other patients

337
Q

What are the indications for receiving a statin?

A
  • All people with established cardiovascular disease (stroke, TIA, IHD, PAD)
  • Anyone with QRISK > 10%
  • Patients with type 1 diabetes who were either diagnosed > 10 years ago OR are aged > 40 OR have established nephropathy
338
Q

When should statins be taken and why?

A

At night, as this is when the majority of cholesterol synthesis occurs

339
Q

Outline primary and secondary prevention statin doses

A

Primary prevention - start at 20mg OD - then if non-HDL has not fallen by > / = 40% then consider titrating up to 80mg

Secondary prevention - atorvastatin 80mg OD

340
Q

What are the electrolyte abnormalities in tumour lysis syndrome?

What other major bloods abnormality will be found?

A
  • High potassium
  • High phosphate
  • High urate
  • Low calcium

AKI

341
Q

What is done for prevention of tumour lysis syndrome?

A
  • IV fluids
  • Patients at higher risk should receive either allopurinol or rasburicase
  • Note both should not be co-administered due as this reduces the effect of rasburicase
342
Q

What is the grading system for tumour lysis syndrome?

A

Cairo-Bishop scoring system
Abnormality in two or more of the following, occurring within three days before or seven days after chemotherapy:
- Uric acid > 475umol/l or 25% increase
- Potassium > 6 mmol/l or 25% increase
- Phosphate > 1.125mmol/l or 25% increase
- Calcium < 1.75mmol/l or 25% decrease

343
Q

How is clinical tumour lysis syndrome defined?

A

Laboratory tumour lysis syndrome plus one or more of the following:
- Increased serum creatinine (1.5x upper limit of normal)
- Cardiac arrythmia or sudden death
- Seizure

344
Q

What can trigger tumour lysis syndrome?

A

Usually related to the treatment of high-grade lymphoma and leukaemias.
- Usually triggered by the introduction of combination chemo
- Can also occur with steroid treatment alone

345
Q

What are the causes of trigeminal neuralgia?

A

Idiopathic
Compression of the trigeminal roots by:
- Tumours
- Vascular problems

346
Q

What are some red flags that could suggest a serious underlying cause in trigeminal neuralgia?

A
  • Sensory changes
  • Deafness or other ear problems
  • History of skin or oral lesions that could spread perineurally
  • Pain only in the ophthalmic division of the trigeminal nerve (eye socket, forehead, and nose), or bilaterally
  • Optic neuritis
  • A family history of multiple sclerosis
  • Age of onset before 40 years
347
Q

What is the management of trigeminal neuralgia?

A
  • Carbamazepine is first line
  • Failure to respond to treatment or atypical features (e.g. < 50yrs) - prompt referral to neurology
348
Q

The sciatic nerve divides into which two other nerves?

A

Tibial and common peroneal nerves

349
Q

Injuries at what site can cause common peroneal nerve lesions?

A

Injuries at the neck of the fibula

350
Q

The common peroneal nerve branches from which other nerve?

A

The sciatic nerve - the sciatic nerve divides into the tibial and common peroneal nerves

351
Q

What is the most characteristic feature in common peroneal nerve lesions?

List some other features of common peroneal nerve lesions

A

Foot drop

Other features:
- Weakness of foot dorsiflexion
- Weakness of foot eversion
- Weakness of extensor hallucis longus
- Sensory loss over the dorsum of the foot and the lower lateral part of the leg
- Wasting of the anterior tibial and peroneal muscles

352
Q

Features of encephalitis?

A
  • Fever, headaches, psychiatric symptoms, seizures, vomiting
  • Focal features e.g. aphasia
  • N.B peripheral lesions e.g. cold sores have no relation to the presence of HSV encephalitis
353
Q

What is the key cause of encephalitis in most cases in adults?

A

HSV-1 is responsible for 95% of cases in adults

354
Q

Where does encephalitis typically occur - which lobes?

A

Temporal and inferior frontal lobes

355
Q

Typical features in neuroimaging in encephalitis?

A
  • Medial temporal and inferior frontal changes (e.g. petechial haemorrhages)
  • Normal in 1/3 of patients
  • MRI is better
356
Q

What is the preferred modality of imaging which is best to pick up changes in encephalitis?

A

MRI

357
Q

What is the classic EEG finding in encephalitis?

A

Lateralised periodic discharges at 2 Hz

358
Q

What is the management in encephalitis?

A

IV aciclovir - in ALL cases of suspected encephalitis

359
Q

What organisms typically cause cellulitis?

A

Strep pyogenes - most common
Staph aureus - next most common

360
Q

What are some criteria for admission for IV antibiotics for cellulitis patients?

A
  • Eron class III or IV
  • Severe or rapidly deteriorating cellulitis (e.g. extensive areas of skin)
  • Very young (< 1 yr) or frail
  • Immunocompromised
  • Significant lymphoedema
  • Facial cellulitis (unless very mild) or periorbital cellulitis
361
Q

What is the classification system used in cellulitis?

A

Eron classification system

I - no signs of systemic toxicity and the person has no uncontrolled co-morbidities
II - the person is either systemically unwell or systemically well but with a co-morbidity (for example peripheral arterial disease, chronic venous insufficiency, or morbid obesity) which may complicate or delay resolution of infection
III - significant systemic upset e.g. acute confusion, tachycardia, tachypnoea, hypotension, or unstable co-morbidities that may interfere with a response to treatment
IV - sepsis or severe life-threatening infection e.g. necrotizing fasciitis

362
Q

Outline the management of cellulitiis as based on the Eron classification system

A

Eron class I
- Oral antibiotics - oral flucloxacillin is first line treatment for mild-moderate cellulitis
- Oral clarithromycin, erythromycin in pregnancy or doxycycline is recommended in patients allergic to penicillin

Eron class II
- Admissino may not be necessary if have the facilities for giving IV antibiotics in the community

Eron class III-IV
- Admit
- Oral / IV co-amoxiclav, oral / IV clindamycin, IV cefuroxime or IV ceftriaxone

363
Q

Patient on immunosuppresive medications post renal transplant - they are at risk in particular of developing which malignancy?

A

SCC of the skin

364
Q

When to add steroids in post-renal transplant regimen?

A

If more than one steroid responsive acute rejection episode

365
Q

What is the mechanism of action of ciclosporin?

A

Calcineurin inhibitor - a phosphotase involved in T-cell activation

366
Q

Some advantages and disadvantages of tacrolimus over ciclosporin?

A

Advantages:
- Lower incidence of acute rejection
- Less hypertension and hyperlipidaemia

Disadvantages:
- High incidence of impaired glucose tolerance and diabetes

367
Q

What is the mechanism of action of MMF?

A

Blocks purine synthesis by inhibition of IMPDH - therefore inhibits proliferation of B and T cells

368
Q

2 key side effects of MMF?

A
  • GI side effects
  • Bone marrow suppression
369
Q

What is the mechanism of action of sirolimus (rapamycin) - a drug used post renal transplant?

A

Blocks T-cell proliferation by blocking the IL-2 receptor

370
Q

What is a key side effect with sirolimus (rapamycin) - a drug used post renal transplant?

A

Hyperlipidaemia

371
Q

What is the mechanism of action of monoclonal antibodies used post renal transplant?
Give examples of these drugs?

A

Selective inhibitors of IL-2 receptor
Daclizumab, basilximab

372
Q

Patients on long term immunosupression for organ transplantation require regular monitoring for complications such as what?

A
  • Cardiovascular diseaes - tacrolimus and ciclosporin can cause HTN and hyperglycaemia. Tacrolimus can cause hyperlipidaemia
  • Renal failure - due to nephrotoxic effects of tacrolimus and ciclosporin / graft rejection / recurrence of original disease in transplanted kidney
  • Malignancy - patients should be counselled to avoid sun exposure to reduce the risk of SCC and BCC of skin
373
Q

What causes secondary hypothyroidism?

A

The only cause is pituituary failure - note this needs pituitary imaging to rule out an anatomical cause such as a tumour or vascular cause

374
Q

Secondary hypothyroidism - caused by pituitary failure, is also associated with which other conditions?

A
  • Down’s syndrome
  • Turner’s syndrome
  • Coeliac disease
375
Q

List causes of primary hypothyroidism

A
  • Hashimotos thyroidism
  • Subacute thyroiditis (De Quervain’s)
  • Riedel’s thyroiditis
  • After thyroidectomy or radioiodene treatment
  • Drug therapy (e.g. lithium, amiodarone or anti-thyroid drugs e.g. carbimazole)
  • Postpartum thyroiditis
  • Dietary iodine deficiency
376
Q

Vitamin A deficiency leads to what condition?

A

Night blindness

377
Q

Which vitamin, if taken in high doses can be dangerous in pregnant women?

A

Vitamin A
Hence why pregnant women are advised not to take multivitamins and not to eat liver

378
Q

How does chancroid typically present?
What organism is it caused by?

A

Painful genital ulcers associated with painful inguinal lymph node enlargement
Ulcers typically have a sharply defined, ragged, undermined border

379
Q

What can happen with suddenly stopping use of long term exogenous corticosteroids?

A

Can precipitate an Addisonian crisis

Because it suppresses the HPA axis, leading to reduced endogenous cortisol production, when suddenly withdrawn, adnreal glands cannot produce enough cortisol to meet the body’s needs, resulting in an Addisonian crisis

380
Q

Place the following corticosteroids - fludrocortisone,dexamethasone, hydrocortisone, betmethasone, prednisolone, in the following categories below:
1) Minimal glucocorticoid activity, very high mineralocorticoid activity
2) Glucocorticoid activity, high mineralocorticoid activity
3) Predominant glucocorticoid activity, low mineralocorticoid activity
4) Very high glucocorticoid activity, minimal mineralocorticoid activity

A

1) Minimal glucocorticoid activity, very high mineralocorticoid activity - Fludrocortisone
2) Glucocorticoid activity, high mineralocorticoid activity - Hydrocortisone
3) Predominant glucocorticoid activity, low mineralocorticoid activity - Prednisolone
4) Very high glucocorticoid activity, minimal mineralocorticoid activity - Dexamethasone, Betmethasone

381
Q

What are the mineralocorticoid side effects of corticosteroids?

A
  • Fluid retention
  • HTN
382
Q

What is the sick day rule for the use of corticosteroids?

A

Patients on long-term steroids should have thir doses doubled during intercurrent illness

383
Q

What are the criteria for tapering down corticosteroids (not how to but when to taper them - in what scenarios)?

A

If patients have:
- Received > 40mg prednisolone daily for > 1 week
- Received > 3 weeks of treatment
- Recently received repeated courses

384
Q

What are the contraindications to BCG vaccination?

A
  • Previous BCG vaccination
  • Past history of TB
  • HIV
  • Pregnancy
  • Positive tuberculin test (Heaf or Mantoux)

Note not given to people > 35 yrs old, as there is no evidence it works for people of this age group

384
Q

Outline the side effects of corticosteroids

A
  • Endocrine - impaired glucose regulation, increased appetite / weight gain, hirsutism, hyperlipidaemia
  • Cushings
  • MSK - osteoporosis, proximal myopathy, AVN femoral head
  • Immunosuppression
  • Pyschiatric - psychosis, insomnia, mania, depressiono
  • GI - peptic ulceration, acute pancreatitis
  • Ophthalmic - glaucoma, cataracts
  • Suppression of growth in children
  • Intracranial HTN
  • Neutrophilia

MR side effects - fluid retention, hypertension

385
Q

In whom should the BCG vaccine be given?

A
  • All infants 0-12 months in areas of the UK where the annual incidence of TB is 10/100 000 or greater
  • All infants 0-12 months with a parent or grandparent who was born in a country where the annual incidence of TB is 40 / 100 000 or greater. Also in older children but they require a tuberculin skin test first
  • Previously unvaccinated tuberculin-negative contacts of cases of respiratory TB
  • Previously unvaccinated, tuberculin negative new entrants under 16 urs who were born in or have lived for a prolonged period (at least 3 months) in a country with an annual TB incidence of 10 / 100 000 or greater
  • Healthcare workers
  • Prison staff
  • Staff of care home for the elderly
  • Those who work with homeless people
386
Q

What do you do first before administering the BCG vaccine? What is the exception?

A

Must first be given the tuberculin skin test. The only exception are children < 6 yrs old who have had no contact with TB

387
Q

Can BCG vaccine be co-administered with other live vaccines?

A

BCG can be given at the same time as other live vaccines, but if not administered simultaneously there should be a 4 week interval

388
Q

How long should the interval be between giving BCG vaccine after another live vaccine (if not given simultaneously at the time)?

A

4 week interval

389
Q

A 34-year-old man is diagnosed as being HIV positive. He was born and brought up in the United Kingdom and is currently fit and well with no past medical history. At what point should anti-retroviral therapy be started?

A) At the time of diagnosis
B) CD4 < 200 x 10^6/L
C) CD4 < 250 x 10^6/L
D) CD4 < 300 x 10^6/L

A

A) At the time of diagnosis

Anti-retroviral therapy is now started at the time of diagnosis, rather than waiting for the CD4 count to drop to a particular level

390
Q

Outline the management of hypercalcaemia

A
  • Initially rehdyration with normal saline - typically 3-4 litres per day
  • Following this bisphosphonates - note they typically take 2-3 days to work with maximal effect being seen at 7 days
  • Other options:
    Calcitonin - quicker effect than bisphosphonates
    Steroids in sarcoidosis

Loop diuretics e.g. furosemide sometimes used, particularly in those who cannot tolerate aggressive fluid rehydration, however they should be used in caution as they may worsen electrolyte derangement and volume depletion

391
Q

What are the features of vestibular schwannoma? Tip base it on the cranial nerves

A

CNV: Absent corneal reflex

CN VIII:
- Vertigo
- Hearing loss (unilateral, sensorineural)
- Tinnitus (unilateral)

CN VII: Facial palsy

392
Q

Bilateral vestibular schwannomas are seen in what condition?

A

Neurofibromatosis type 2

393
Q

What investigations to carry out in vestibular schwanomma?

A

MRI of the cerebellopontine angle
Audiogram

394
Q

What is the management of vestibular schwannoma?

A

Refer to ENT
Either surgery, radiotherapy or observation

395
Q

Infarction in which coronary territory can cause complication of complete heart block following an MI?

A

Right coronary artery lesion

Since this supplies the AVN in most people (90%). Infarction of the AV node leads to loss of the normal conduction pathway from the atria to the ventricles. Well known complication post-MI

396
Q

Outline the different ways that diabetic foot disease can present?

A
  • Neuropathy - loss of sensation
  • Ischaemia - absent foot pulses, reduced ABPI, intermittent claudication
  • Complications: calluses, ulceration, Charcot’s arthropathy, cellulitis, osteomyelitis, gangrene
397
Q

All patients with diabetes should be screened with diabetic foot disease on at least an annual basis - what is done in this testing?

A
  • Screening for ischaemia - palpate both the dorsalis pedis pulse and posterior tibial artery pulse
  • Screening for neuropathy - 10g monofilament on various parts of the sole of the feet
398
Q

Outline the risk stratification for low risk, moderate risk and high risk in diabetic foot disease

A

Low risk - no risk factors except callus alone
Moderate risk - Deformity or …. , neuropathy or…. , non-critical limb ischaemia
High risk - previous ulceration or …, previous amputation… , or on RRT or…, neuropathy and non-critical limb ischaemia together or…., neuropathy in combination with callus and / or deformity or…., criticitcal limb ischaemia in combination with callus and / or deformity

Note all patients who are moderate or high risk (i.e. any problems other than simple calluses) should be followed up regularly by the local diabetic foot centre

399
Q

What is the most prevalent STI in the UK?

A

Chlamydia trachomatis

400
Q

What is the incubation period of chlamydia trachomatis?

A

7-21 days

401
Q

What are the clinical features of chlamydia?

A
  • Asymptomatic in around 70% of women and 50% of men
  • Women: cervicitis (discharge, bleeding), dysuria
  • Men: urethral discharge, dysuria
402
Q

List some complications of chlamydia trachomatis:

A
  • Epididymitis
  • PID
  • Endometritis
  • Increased incidence of ectopic pregnancies
  • Infertility
  • Reactive arthritis
  • Perihepatitis (Fitz-Hugh-Curtis syndrome)
403
Q

When should chlamydia testing be carried out?

A

Two weeks after a possible exposure

404
Q

What are the investigations carried out in chlamydia trachomatis?

A

NAATs - urine, vulvovaginal swab or cervical swab

For women - vulvovaginal swab NAAT is first line
For men - urine NAAT is first line

405
Q

What is the screening programme in Chlamydia in the UK?

A

Open to all men and women aged 15-24 years

406
Q

1) What is the first line management for chlamydia?
2) What if this is contraindicated or not tolerated?
3) What should be used in pregnant women?

A

1) Doxycycline - 7 day course
2) If contraindicated / not tolerated - azithromycin - either 1g OD or 500mg OD for two days
3) If pregnant - azithromycin, erythromycin, amoxicillin - 1g azithromycin first line following discussion or risk vs benefit

407
Q

What are the notification protocols in chlamydia?

A
  • For men with urethral symptoms:
    All contacts since, and in the four weeks prior to the onset of symptoms
  • For women and asymptomatic men:
    All partners from the last six months or the most recent sexual partner should be contacted
  • Contacts of confirmed chlamydia cases should be offered treatment prior to hte results of their investigations being known (treat then test)
408
Q

Outline when blood pressure should be controlled in acute stroke patients

Blood pressure should be lowered to what before thrombolysis?

A
  • BP should not be lowered in the acute phase of ischaemic stroke unless there are complications e.g. Hypertensive encephalopathy or being considered for thrombolysis
  • BP control should be considered for patients who present with an acute ischaemic stroke, if they present within 6 hours and have a systolic BP > 150mmHg

BP should be lowered to 185/110 mmHg before thrombolysis

409
Q

What medication and what dose should be given for acute ischaemic stroke?

A

Aspirin 300mg orally or rectally ASAP if a haemorrhagic stroke has been excluded

410
Q

When can you restart anticoagulants following an ischaemic stroke in patients with AF?

A

Anticoagulants should not be started until brain imaging has excluded haemorrhage, and usually not until 14 days have passed from the onset of an ischaemic stroke

411
Q

When can patients be started on statin following ischaemic stroke if needed - and in whom is it needed?

A

If cholesterol is > 3.5 mmol/L then patients should be commenced on a statin
Often delay treatment until at least 48 hours due to risk of haemorrhagic transformation

412
Q

What are the criteria for thrombolysis with alteplase or tenecteplase?

A
  • Administered within 4.5 hrs of onset - or if treatment can be started between 4.5 and 9 hrs of known onset, or within 9 hours of midpoint of sleep when they have woken with symptoms AND
    -The have evidence from CT / MR perfusion (core-perfusion mismatch) or MRI (DWI-FLAIR mismatch) of the potential to salvage brain tissue
  • This should be irrespective of whether they have a large artery occlusion and require mechanical thrombectomy
  • Haemorrhage has been definitively excluded (i.e. imaging has been performed)
413
Q

What are the guidelines for overall clinical status of a patient when considering for thrombectomy?

A

Pre-stroke functional status of < 3 on the modified Rankin scale and a score of > 5 on the NIHSS

414
Q

When to consider thrombectomy +/- IV thrombolysis?

A

Offer thrombectomy ASAP and within 6 hours of symptom onset, together with IV thrombolysis (if within 4.5 hours), to people who have:
Acute ischaemic stroke and
- Confirmed occlusion of the proximal anterior circulation demonstrated by CTA or MRA

Offer thrombectomy ASAP to people known to be well between 6-24 hours previously (including wake-up strokes):
- Confirmed occlusion of the proximal anterior circulation demonstrated by CTA or MRA and
- If there is potential to salvage brain tissue, as shown by imaging such as CT perfusion or diffusion weighted MRI sequences showing limited infarct core volume

Consider thrombectomy with IV thrombolysis (if within 4.5 hours) as soon as possible for people last known to be well up to 24hrs previously (including wake-up strokes)
- who have acute ischaemic stroke and confirmed occlusion of the proximal posterior circulation (i.e. basilar or posterior cerebral artery) demonstrated by CTA or MRA and…
- if there is potential to salvage brain tissue as shown by CT perfusion or diffusion-weighted MRI sequences showing limited infarct core volume

415
Q

What is given for lifelong treatment for secondary prevention of stroke? What is given if this is not tolerated?

A
  • Clopidogrel lifelong
  • Or aspirin + dipyridamole if clopidogrel not tolerated
416
Q

When should carotid endarterectomy given in stroke?

A
  • If suffered stroke or TIA in the carotid territory
  • Not severely disabled
  • If stenosis > 50%
417
Q

Outline the medical management of angina pectoris (stable)

A
  • Aspirin + statin in the absence of any contraindication
  • Sublingual GTN to abort angina attacks
  • Either a beta-blocker or CCB first-line based on comorbidities, contraindications and the person’s preference
  • If a CCB is used monotherapy use a rate-limiting one e.g. verapamil or diltiazem
  • If used in combination with beta-blocker then use longer acting dihydropyridine CCB (e.g. amlodipine, modified release nifedipine). Do NOT co-prescribe beta-blockers and verapamil - risk of complete heart block
  • If poor response to initial therapy increase to max tolerated dose
  • If still symptomatic after monotherpay with beta-blocker add a CCB and vice versa
  • If on monotherapy and cannot tolerate a second drug (either CCB or beta-blocker) then consider andy of : long acting nitrate, ivabradine, nicorandil, ranolazine
  • If a patient is taking both CCB and beta-blocker then only add a third drug when awaiting assessment for PCI or CABG
418
Q

How to manage nitrate tolerance in patients taking isosorbide mononitrate?

A

NICE advises that patients who take standard-release isosorbide mononitrate should use an asymmetric dosing interval to maintain a daily nitrate-free time of 10-14 hours to minimise the development of nitrate tolerance
this effect is not seen in patients who take once-daily modified-release isosorbide mononitrate

419
Q

Lyme disease is caused by which organism and is spread by what?

A

Borriela Burgdorferi
Spread by ticks

420
Q

Features of lyme disease?

A
  • Erythema migrans - in 80% of patients
  • Systemic features - headache, lethargy, fever, arthralgia
  • Cardiovascular - heart block, peri/myo-carditis
  • Neuro - facial nerve palsy, radicular pain, meningitis
421
Q

Investigations in Lyme disease?

A

NICE recommend that Lyme disease can be diagnosed clinically if erythema migrans is present

Enzyme-linked immunosorbent assay (ELISA) antibodies to Borrelia burgdorferi are the first-line test

  • If negative and Lyme disease is still suspected in people tested within 4 weeks from symptom onset, repeat the ELISA 4-6 weeks after the first ELISA test
  • If still suspected in people who have had symptoms for 12 weeks or more then an immunoblot test should be done
  • If positive or equivocal then an immunoblot test for Lyme disease should be done
422
Q

What is the management of Lyme disease?

A
  • Doxycyline if early disease
  • Amoxicillin if doxy is contraindicated (e.g. pregnancy)
  • Ceftriaxone if disseminated disease
  • Jarisch-Herxheimer reaction is sometimes seen after initiating therapy: fever, rash, tachycardia after first dose of antibiotic (more commonly seen in syphilis, another spirochaetal disease)
423
Q

What reaction can sometimes happen after initiating therapy in Lyme disease?
In which other condition can this happen also?

A

Jarisch-Herxheimer reaction - fever, rash, tachycardia after first dose of antibiotic (more commonly seen in syphilis, another spirochaetal disease)

424
Q

What score system can be used in assessment of considering whether stroke is likely?

A

ROSIER score

Exclude hypoglycaemia first then….

Loss of consciousness - NEGATIVE 1 point
Seizure activity - NEGATIVE 1 point
New acute onset of:
- Asymmetric facial weakness - + 1 point
- Asymmetric arm weakness - + 1 point
- Asymmetric leg weakness - + 1 point
- Speech disturbance - + 1 point
- Visual field defect - +1 point

Stroke likely if > 0 points

425
Q

What is the most common cause of primary hypoadrenalism in the UK?

A

Addison’s - autoimmune destruction of the adrenal glands
80% of cases

426
Q

Features of Addison’s disease

Features of Addisonian crisis?

A
  • lethargy, weakness, anorexia, nausea & vomiting, weight loss, ‘salt-craving’
  • hyperpigmentation (especially palmar creases)
  • vitiligo
  • loss of pubic hair in women
  • hypotension
  • hypoglycaemia
  • hyponatraemia and hyperkalaemia may be seen

Crisis: collapse, shock, pyrexia

427
Q

List causes of primary hypoadrenalism

A
  • Most common - Addisons (autoimmune destruction of adrenals)
  • TB
  • Metastases (e.g. bronchial carcinoma)
  • HIV
  • Antiphospholipid syndrome
428
Q

List secondary causes of hypoadrenalism

A

Pituitary disorders - tumours, irradiation, infiltration
Exogenous glucocorticoid therapy

429
Q

What type of bacteria is Neisseria Gonorrhae - gram -ve or positive and rod or coccus?

A

Gram negative diplococcus

430
Q

What is the incubation period of gonorrhoea?

A

2-5 days

431
Q

Features of gonorrhoea?

A
  • Males - urethral discharge, dysuria
  • Females - cervicitis e.g. leading to vaginal discharge
  • Rectal and pharyngeal infection usually asymptomatic
432
Q

True or false, no vaccination exists for gonorrhoea?

A

True - immunisation is not possible and reinfection is common due to antigen variation of type IV pili (proteins which adhere to surfaces) and Opa proteins (surface proteins which bind to receptors on immune cells)

433
Q

Complications of gonorrhoea?

A
  • Urethral strictures
  • Epididymitis
  • Salpingitis (hence may lead to infertility)
  • Disseminated infection - tenosynovitis, migratory polyarthritis, dermatitis (lesions may be maculopapular or vesicular). Later complications septic arthritis, endocarditis, perihepatitis (Fitz-Hugh-Curtis syndrome)
434
Q

What is first line treatment for gonorrhoea?

What if this is not tolerated?

A

Single dose of IM ceftriaxone 1g
If sensitive to cipro - single dose of oral cipro 500mg

If ceftriaxone is refused (e.g. needle phobic) then oral cefixime 400mg (single dose) + oral azithromycin 2g (single dose) should be used

435
Q

Pathogen associated with bronchiolitis?

A

Respiratory syncytial virus

436
Q

Pathogen associated with croup?

A

Parainfluenza virus

437
Q

Most common pathogen behind CAP?

A

Strep pneumoniae

438
Q

Pathogen that can cause CAP, is the most common cause of bronchiectasis exacerbations, acute epiglottitis?

A

Haemophilus influenzae

439
Q

Which pathogen commonly associated with pneumonia following influenza?

A

Staph aureus

440
Q

Which pathogen in pneumonia can be complicated by haemolytic anaemia and erythema multiforme?

A

Mycoplasma pneumoniae

441
Q

Which pathogen in pneumonia can be complicated by lymphopaenia, deranged LFTs and hyponatraemia?

A

Legionella pneumonia

442
Q

What should you advise for renal diet for patients with renal failure? Low what (not just one thing btw)

A
  • Low protein
  • Low phosphate
  • Low sodium
  • Low potassium
443
Q

Outline treatment in acute heart failure?

A
  • IV loop diuretics - e.g. furosemide, bumetanide
  • Oxygen - aim sats 94-98% (unless COPD?)
  • Vasodilators - NOT routinely - only if concomitant myocardial ischaemia, severe hypertension, or regurgitant aortic or mitral valve disease - CI in hypotension
  • Resp failure - CPAP NOT Bipap
  • HOTN (e.g. < 85mmHg / cardiogenic shock)
    Inotropic agents e.g. dobutamine - for patients with severe LV dysfunction who have potentially reversible cardiogenic shock, vasopressor agents e.g. norepinephrine - if insufficient response to inotropes and evidence of end-organ hypoperfusion, mechanical circulatory assistance e.g. intra-aortic ballon counterpulsation or ventricular assist devices
444
Q

When should beta-blockers be stopped in patients who take them for heart failure in the acute heart failure scenario?

A

Beta-blockers should not be stopped if the patient has heart rate < 50 bpm, second or third degree AV block, or shock

445
Q

List causes of vitamin B12 deficiency

A
  • Pernicious anaemia - most common cause
  • Post gastrectomy
  • Vegan diet or poor diet
  • Disorders / surgery of terminal ileum - Crohns either disease activity or following ileocaecal resection
  • Metformin (rare)
446
Q

List some features of vitamin B12 deficiency

A
  • Macrocytic anaemia
  • Sore tongue and mouth
  • Neurological symptoms
    the dorsal column is usually affected first (joint position, vibration) prior to distal paraesthesia
  • Neuropsychiatric symptoms: e.g. mood disturbances
447
Q

Outline management of vitamin B12 deficiency

A
  • If no neurological involvement 1 mg of IM hydroxocobalamin 3 times each week for 2 weeks, then once every 3 months
  • If a patient is also deficient in folic acid then it is important to treat the B12 deficiency first to avoid precipitating subacute combined degeneration of the cord
448
Q

GBS often triggered by infection with which organism?

A

Campylobacter Jejuni

449
Q

Features of Miller Fisher syndrome?

A
  • Descending paralysis rather than ascending paralysis in GBS
  • Ophthalmoplegia
  • Areflexia
  • Ataxia
450
Q

Which antibodies are present in 90% of cases of GBS?

A

Anti-GQ1b antibodies

451
Q

Features of trichomonas vaginalis?

A

vaginal discharge: offensive, yellow/green, frothy
vulvovaginitis
strawberry cervix
pH > 4.5
in men is usually asymptomatic but may cause urethritis

452
Q

Management of Trichomonas Vaginalis?

A

Oral metronidazole 5-7 days
Or one off 2g metronidaole

453
Q

What is the investigation in suspected trichomonas vaginalis?

A

Microscopy of a wet mount shows motile trophozoites

454
Q

What is Buerger’s disease and what are the features of it?

A

Buerger’s disease (also known as thromboangiitis obliterans) is a small and medium vessel vasculitis that is strongly associated with smoking

Features:
- Extremity ischaemia
- Intermittent claudication
- Ischaemic ulcers
- Superficial thrombophlebitis
- Raynaud’s phenomenon

455
Q

Buerger’s disease is strongly associated with what key risk factor?

A

Smoking

456
Q

Most common bacterial causes of acute exacerbations of COPD?

A
  • Haemophilus influenzae - MOST COMMON
  • Streptococcus pneumoniae
  • Moraxella catarrhalis
457
Q

Which respiratory virus is the most common in acute exacerbation of COPD?

A

Human rhinovirus

458
Q

Initial management of acute exacerbation of COPD? i.e. not severe, not requiring hospital admission

A
  • Increase the frequency of bronchodilator use and consider giving via a nebuliser
  • Give prednisolone 30mg OD for 5 days
  • Only give abx (amoxicillin / clarithromycin / doxycycline) IF sputum is purulent or clinical signs of pneumonia
459
Q

Indications for admission for acute exacerbation of COPD?

A
  • Severe breathlessness
  • Acute confusion or impaired consciousness
  • Cyanosis
  • Oxygen sats < 90% on pulse ox
  • Social reasons e.g. inability to cope at home (or living alone)
  • Significant comorbidity (e.g. cardiac disease or insulin-dependent diabetes)
460
Q

How to titrate oxygen therapy in management of COPD?

A
  • Initial targets of 88-92%
  • Prior to the availability of blood gases, use a 28% Venturi mask at 4L/min and aim for O2 sats of 88-92% for patients with risk factors for hypercapnia but no prior history of respiratory acidosis
  • Adjust target range to 94-98% if the PCO2 is normal
461
Q

Outline management options for severe COPD

A
  • Oxygen therapy
  • Nebulised bronchodilator therapy
    Beta-adrenergic agonist e.g. salbutamol
    Muscarinic antagonist e.g. ipratropium
  • Steroid therapy - Oral prednisolone or IV hydrocortisone
  • IV theophylline - if not responding to nebulised bronchodilators
  • IF resp aciosis NIV , consider HDU
    BIPAP
    EPAP 4-5cm H20
    IPAP either 10cm H20 or 12-15cm H20
462
Q

What are the commonest causes of anterior mediastinum mass?

A

4 T’s: Teratoma, Terrible lymphadenopathy, Thymic mass and Thyroid mass

463
Q

What is the management for SVT in shock?

A

Synchronised DC cardioversion

Note when you can feel a measurable pulse its synchronised e.g. SVT in shock but if either VF/VT/pulseless with shock then its unsynchronised

464
Q

What is raised in the FBC in polycythaemia vera?

A
  • Hb main thing but also accompanied by…
  • Neutrophils
  • Platelets
465
Q

Incidence of polycythaemia vera is greatest when?

A

In the sixth decade

466
Q

Features of polycythaemia?

A
  • Pruritus, typically after a hot bath (aquagenic pruritis)
  • Splenomegaly
  • Hypertension
  • Hyperviscosity - Arterial thrombosis / Venous thrombosis
  • Haemorrhage (secondary to abnormal platelet function)
  • Low ESR
467
Q

Investigations in suspected polycythaemia vera?

A

full blood count/film (raised haematocrit; neutrophils, basophils, platelets raised in half of patients)
JAK2 mutation
serum ferritin
renal and liver function tests

If the JAK2 mutation is negative and there is no obvious secondary causes the BCSH suggest the following tests:
red cell mass
arterial oxygen saturation
abdominal ultrasound
serum erythropoietin level
bone marrow aspirate and trephine
cytogenetic analysis
erythroid burst-forming unit (BFU-E) culture

468
Q

Diagnostic criteria for polycythaemia rubra vera?

A
469
Q

Main mechanism of action of metoclopramide?

A

D2 receptor antagonist

470
Q

Uses of metoclopramide?

A
  • Anti-emetic
  • GORD
  • Prokinetic action useful in gastroparesis secondary to diabetic neuropathy
  • Often combined with analgaesics for treatment of migraine (migraine attacks result in gastroparesis, slowing the absorption of analgaesics)
471
Q

Adverse effects associated with metoclopramide?

A
  • Extrapyramidal effects - acute dystonia e.g. oculogyric crisis - especially in children and young adults
  • Diarrhoea
  • Hyperprolactinaemia
  • Tardive dyskinesia
  • Parkinsonism
472
Q

Metoclopramide should be avoided in …. ….., but may be helpful in paralytic ileus

A

Metoclopramide should be avoided in bowel obstruction, but may be helpful in paralytic ileus

473
Q

Metoclopramide should be avoided in bowel obstruction, but may be helpful in ….. …..

A

Metoclopramide should be avoided in bowel obstruction, but may be helpful in paralytic ileus

474
Q

Causes AR - both due to valve disease and aortic root disease and chronic vs acute in these?

A
475
Q

Features of aortic regurgitation?

A
  • Early diastolic murmur: intensity of the murmur is increased by the handgrip manoeuvre
  • Collapsing pulse
  • Wide pulse pressure
  • Quincke’s sign (nailbed pulsation)
  • De Musset’s sign (head bobbing)
    mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams
476
Q

Indications for surgical management of aortic regurgitation?

A
  • Symptomatic patients with AR
  • Asymptomatic patients with severe AR who have LV systolic dysfunction
477
Q

Adverse effects associated with nicorandil?

A
  • Headaches
  • Flushing
  • Skin, mucosal, eye and anal ulceration
478
Q

Contraindication for nicorandil?

A

Left ventricular

479
Q

What is the peak incidence of Bell’s palsy?
In what group of people is it most common?

A

20-40yrs
Pregnant women

480
Q

Features of facial palsy?

A
  • Lower motor neuron facial nerve palsy → forehead affected
    in contrast, an upper motor neuron lesion ‘spares’ the upper face

Patients may also notice:
- post-auricular pain (may precede paralysis)
- altered taste
- dry eyes
- hyperacusis

481
Q

Management for Bell’s palsy?

A
  • Oral pred within 72 hours
  • Aciclovir IF severe facial palsy
  • Eye care and artificial tears, micropore tape
  • IF no improvement after 3 weeks - refer to ENT
  • IF more longstanding weakness e.g. 3 months - refer to plastic surgery
482
Q

Prognosis of Bell’s palsy?

A

Most recover in 3-4 months
If untreated around 15% have permanent moderate to severe weakness

483
Q

Typhoid and paratyphoid are caused by which organisms respectively?

A

Salmonella Typhi and Salmonella Paratyphi

484
Q

Features of enteric fever (typhoid / paratyphoid)?

A
  • Systemic upset - headache, fever, arthralgia
  • Relative bradycardia
  • Abdominal pain, distension
  • Constipation - although salmonella is a recognised cause of diarrhoea, constipation is more common in typhoid
  • Rose spots - present on the trunk in 40% of patients, and are more common in paratyphoid
485
Q

Possible complications of enteric fever - typhoid / paratyphoid?

A
  • Osteomyelitis (especially in sickle cell disease where Salmonella is one of the most common pathogens)
  • GI bleed / perforation
  • Meningitis
  • Cholecystitis
  • Chronic carriage (1% more likely if adult females)
486
Q

What infections can Pseudomonas Aeruginosa cause?

A
  • Chest infections (especially in cystic fibrosis)
  • Skin: burns, wound infections, ‘hot tub’ folliculitis
  • Otitis externa (especially in diabetics who may develope malignant otitis externa)
  • UTIs
487
Q

Pseudomonas aeruginosa gram -ve or positive and rod or bacillus?

A

Gram -ve rod

488
Q

Lab features of Pseudomonas Aeruginosa?

A
  • Gram-negative rod
  • Non-lactose fermenting
  • Oxidase positive
489
Q

A 31-year-old male presents to his GP complaining of a sudden onset 3 day history of fever, shivers and a sore throat. He has a past medical history of ulcerative colitis, for which he is treated with the aminosalicylate, mesalazine.

What is the most important investigation in this patient?

A) Blood cultures
B) FBC
C) LFTs
D) U+Es
E) Viral throat swab

A

FBC - Aminosalicylates, such as sulphasalazine or mesalazine have a number of side effects. Mesalazine, in particular, can cause agranulocytosis, which may present with sudden onset rigors, fever and sore throat

490
Q

List differentials for melaena in terms of oesophageal, gastric and duodenal causes

A

OESOPHAGEAL:
- Oesophageal varices
- Oesophagitis
- Cancer
- Mallory-Weiss Tear

GASTRIC:
- Gastric ulcer
- Gastric cancer
- Dieulafoy lesion
- Diffuse erosive gastritis

DUODENAL CAUSES:
- Duodenal ulcer
- Aorto-enteric fistula

491
Q

What scoring system in upper GI bleeds is used before endoscopy at first assessement and what is used after endoscopy to provide a percentage risk of rebleeding and mortality?

A
  • Glasgow-Blatchford Score - at first assessment - helps decide whether patients can be managed as outpatients or not, and urgency of endoscopy
  • Rockall Score - after endoscopy - after endoscopy provides a percentage risk of rebleeding and mortality
492
Q

What Glasgow-Blatchford score may be considered for early discharge?

A

0

493
Q

What blood products are used in management of upper GI bleeds?

A

Beware transfusing too much RBC due to increase in portal venous pressure

  • Platelet transfusion if actively bleeding platelet count of less than 50 x 10*9/litre
  • Fresh frozen plasma to patients who have either a fibrinogen level of less than 1 g/litre, or a prothrombin time (international normalised ratio) or activated partial thromboplastin time greater than 1.5 times normal
  • Prothrombin complex concentrate to patients who are taking warfarin and actively bleeding
494
Q

Outline the management of variceal bleeding in upper GI bleeding?

A
  • Terlipressin and prophylactic antibiotics should be given to patients at presentation (i.e. before endoscopy)
  • Band ligation should be used for oesophageal varices and injections of N-butyl-2-cyanoacrylate for patients with gastric varices
  • Transjugular intrahepatic portosystemic shunts (TIPS) should be offered if bleeding from varices is not controlled with the above measures
495
Q

Outline the management of non-variceal upper GI bleeding?

A
  • NICE do not recommend the use of proton pump inhibitors (PPIs) before endoscopy to patients with suspected variceal upper gastrointestinal bleeding although PPIs should be given to patients with non-variceal upper gastrointestinal bleeding and stigmata of recent haemorrhage shown at endoscopy
  • If further bleeding then options include repeat endoscopy, interventional radiology and surger
496
Q

Name 3 of the most common precipitating factors of DKA?

A
  1. Infection
  2. Missed insulin doses
  3. MI
497
Q

What are the diagnostic criteria for DKA?

A

American Diabetes Association:
- Glucose > 13.8 mmol/l
- pH < 7.30
- Serum bicarbonate <18 mmol/l
- Anion gap > 10
- Ketonaemia

Joint British Diabetes Societies (2013):
- Glucose > 11 mmol/L or known diabetes mellitus
- pH < 7.3
- Bicarbonate < 15 mmol/L
- Ketones > 3 mmol/L or urine ketones ++ on dipstick

498
Q

DKA resolution is defined as ….?

A
  • pH >7.3 and
  • blood ketones < 0.6 mmol/L and
  • bicarbonate > 15.0mmol/L
499
Q

List some complications of DKA

A
  • Gastric stasis
  • Thromboembolism
  • Arrhythmias secondary to - Hyperkalaemia/iatrogenic hypokalaemia
  • Iatrogenic due to incorrect fluid therapy: cerebral oedema*, hypokalaemia, hypoglycaemia
  • Acute respiratory distress syndrome
  • Acute kidney injury
500
Q

Which demographic is particular at risk of complications from fluid therapy in DKA, what is the complication, and how to mitigate the risk?

A

Children / young adults are particularly vulnerable to cerebral oedema following fluid resuscitation in DKA and often need 1:1 nursing to monitor neuro-observations, headache, irritability, visual disturbance, focal neurology etc. It usually occurs 4-12 hours following commencement of treatment but can present at any time. If there is any suspicion a CT head and senior review should be sough

501
Q
A

MSRA (2 decks)

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