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MSRA > Medicine > Flashcards

Medicine Flashcards

1
Q

Patient presents with painful, hot, erythematous area on his anterior shin. Systemically well. What oral treatment with penicillin allergy?

A

Clarithromycin

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2
Q

What is cellulitis

A

Inflammation of the skin and subcutaneous tissue?

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3
Q

What are the main organisms that cause cellulitis?

A

Streptococcus Pyogenes

Staphylococcus Aureus

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4
Q

What is the criteria for admission for Cellulitis?

A

Eron Classification

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5
Q

What is Class 1 for the Eron Classification?

A
  • No signs of systemic toxicity

- no uncontrolled co-morbidities

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6
Q

What is Class 2 for Eron Classification?

A
  • systemically unwell
  • Systemically well but with a co-morbidity (PVD, chronic venous insufficiency, morbid obesity) which may complicate or delay resolution of infection
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7
Q

What is Class 3 of Eron Classification?

A
  • significant systemic upset (acute confusion, tachycardia, tachypnoea, hypotension, unstable co-morbidities)
  • Limb threatening infection due to vascular compromise
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8
Q

What is Class 4 Eron Classification?

A

Sepsis syndrome

Life threatening infection e.g necrotising fasciitis

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9
Q

What is the admission criteria for cellulitis for IV antibiotics?

A
  • Eron III or IV
  • Severe or rapidly deteriorating cellulitis
  • Very young (<1yr)
  • Very old
  • Immunocompromised
  • Significant Lymphoedema
  • Facial cellulitis
  • Periorbital cellulitis
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10
Q

What can be considered in some cases for Eron Class II?

A
  • May not be necessary if facilities and expertise are available in the community to give IV Abx and monitor patient
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11
Q

What is the first line management for mild-moderate cellulitis?

A

Flucloxacillin

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12
Q

What is the first line management for Pen-allergy mild to moderate cellulitis?

A

Clarithromycin
Erythromycin (pregnancy)
Doxycycline

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13
Q

What should be given to patients with severe cellulitis?

A

Co-amoxiclav
Cefuroxime
Clindamycin
Ceftriaxone

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14
Q

Man admitted with palpitations without chest pain, normal tachycardia and ECG demonstrates regular, monomorphic, broad complex tachycardia. Nil features of myocardial ischaemia.

A

Ventricular Tachycardia

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15
Q

What does the European Resuscitation Council advise in with a broad complex tachycardia in a peri-arrest situation?

A

Assume this is ventricular in origin

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16
Q

What is the first step of Resus Council assessment of a tachycardia?

A

Give O2
IV Access
Monitor ECG BP O2 record ECG
Treat reversible causes

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17
Q

What is the next step of the resus council assessment of tachycardia?

A 
Are there life-threatening features present? 
Shock 
Syncope
MI 
Severe Heart Failure
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18
Q

What to do if the answer to step 2 (shock/syncope/MI/ Severe HF) present?

A 
Synchronised DC shock up to 3 attempts 
- Sedation or anaesthesia if conscious 
If unsuccessful 
- Amiodarone 300mg IV over 10-20mins
- Repeat synchronised DC shock
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19
Q

What is the management of tachycardia if there is no life threatening features present?

A

Is the QRS narrow?

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20
Q

What is the management of narrow QRS Tachycardia?

A

Is it regular or irregular?

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21
Q

What is the management of regular, narrow QRS tachycardia?

A

Vagal Manoeuvres
Then consider
- Adenosine (if no pre-excitation) 6mg, 12mg, 18mg
Monitor ECG continuously

If ineffective
Give Verapamil or beta-blocker

Then consider synchronised DC shock up to 3 attempts

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22
Q

What is the management of irregular, narrow QRS?

A

Likely atrial fibrillation

  • Rate control with beta-blocker
  • Consider digoxin or amiodarone if evidence of heart failure
  • Anticoagulate if duration >48hrs
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23
Q

What is the management of regular, broad complex tachycardia?

A

If VT or uncertain rhythm
- Give amiodarone 300mg IV over 10-60mins ideally through a central line
?consider lidocaine (use with caution in severe LV impairment)
Procainamide

If previous certain diagnosis of SVT with bundle branch block/aberrant conduction?
- treat as for regular narrow complex tachycardia

If not successful consider
- Synchronised DC shock 3 attempts with sedation/anaesthesia

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24
Q

What should not be used in the management of VT?

A

verapamil

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25
Q

What is the differential of irregular broad complex tachycardia?

A

Atrial Fibrillation with BBB treat as irregular narrow complex
Could be polymorphic VT (torsades) - give MgSO4 over 10 mins.

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26
Q

Why is verapamil contraindicated in VT?

A

This is because IV administration of Ca Channel blockers can precipitate cardiac arrest

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27
Q

What do you offer patients with advanced and progressive disease in palliative care?

A

Regular Oral MR morphine OR

Regular Immediate-Release Morphine with oral IR morphine for breakthrough pain

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28
Q

For palliative patients with advanced/progressive disease with NO comorbidities how much morphine should you use?

A

20-30mg of MR a day
5mg morphine for breakthrough pain

eg. 15mg MR morphine BD with 5mg oral morphine PRN

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29
Q

What should oral MR morphine be used instead of?

A

Transdermal patches

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30
Q

What must be prescribed to all patients on strong opioids?

A

Laxatives

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31
Q

What symptoms are usually transient with opioids?

A

Nausea - if persistent antiemetic

Drowsiness - consider dose adjustment if ongoing

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32
Q

How should breakthrough dose for pain control in adults with cancer be calculated?

A

1/6 daily dose of morphine

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33
Q

How should pain management be adjusted in adults with cancer with CKD?

A

Opioids should be used with caution
- Oxycodone is preferred to morphine in palliative patients with mild-moderate renal impairment

If severe renal impairment
- consider alfentanil, buprenorphine, fentanyl

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34
Q

What is the management of metastatic bone pain

A

Strong Opioids
Bisphosphonates
Radiotherapy

All patients should be considered for referral for radiotherapy

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35
Q

For palliative care pain patients when considering increasing dose of opioids how much increase should you consider?

A

30-50%

Consider bisphosphonates, radiotherapy, denosumab

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36
Q

How do you convert from Oral Codeine to Oral Morphine?

A

Divide by 10

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37
Q

How do you convert from Oral tramadol to oral morphine

A

Divide by 10 (previously stated as 5 but current version states 10)

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38
Q

How do you convert from oral morphine to oral oxycodone?

A

Divide by 1.5-2 (causes less sedation, vomiting and pruritis than morphine)

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39
Q

How much does a transdermal fentanyl 12 microgram patch equate to in oral morphine?

A

30mg

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40
Q

How much does a transdermal buprenorphine 10 microgram patch equate to in oral morphine?

A

24mg

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41
Q

How do you convert from oral morphine to subcut morphine?

A

Divide by 2

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42
Q

How do you convert from oral morphine to subcut diamorphine?

A

Divide by 3

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43
Q

How do you convert from oral oxycodone to subcut diamorphine?

A

Divide by 1.5

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44
Q

What is the general rule for management of migraines for acute treatment vs prophylaxis?

A

5-HT receptor agonist for acute treatment

5-HT receptor antagonist for prophylaxis

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45
Q

What is the acute, first-line treatment for migraine?

A

Combination therapy

- Oral triptan, NSAID or oral triptan and paracetamol

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46
Q

What is an example of a 5-HT receptor agonist?

A

Sumatriptan

Rizatriptan

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47
Q

What can be considered for acute treatment of migraine in young people aged 12-17?

A

Nasal triptan in preference to oral triptan

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48
Q

What is the next step of acute management of migraine following triptans/paracetamol?

A

Consider metoclopramide

Prochlorperazine and consider adding non-oral NSAID/Triptan

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49
Q

When should you consider migraine prophylaxis for patients

A

Patient experiencing 2 or more attacks a month - effective in 60% of patients

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50
Q

What is the first line prophylaxis of migraine in patients?

A

Topiramate

Propranolol

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51
Q

When would you use propranolol over topiramate?

A

Women of child bearing age as it may be teratogenic and can reduce effectiveness of hormonal contraceptives?

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52
Q

What is the next step of management if propranolol or topiramate fail in migraine prophylaxis?

A

A course of up to 10 sessions of acupuncture over 5-8 weeks?
Advise riboflavin 40mg may be effective

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53
Q

What is the management of migraine in patients with predictable menstrual migraine treatment?

A

Frovatriptan (2.5mg BD)
Zolmitriptan (2.5mg BD/TDS)
- Mini-prophylaxis

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54
Q

Why is pizotifen not routinely recommended in migraine prophylaxis?

A

Adverse effects

  • Weight gain
  • Drowsiness
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55
Q

What is the first line management of stable angina?

A

All patients should receive aspirin and a statin in the absence of any contraindications

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56
Q

What medication can be used to abort angina attacks?

A

GTN - Glyceryl Trinitrate

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57
Q

75yr old with AF, BP 128/80 - drug to control heart rate?

A

Bisoprolol

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58
Q

When should rate control not be offered first-line for atrial fibrillation?

A
  • Reversible cause
  • Heart failure primarily caused by AF
  • New-onset AF (<48hr)
  • AF considered suitable for an ablation strategy to restore
  • Where rhythm control strategy would be more suitable on clinical judgement
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59
Q

What medications are used to treat Atrial Fibrillation?

A

Beta-Blocker
CCB
Digoxin

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60
Q

When are beta-blockers contra-indicated?

A

Asthma

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61
Q

When is digoxin considered for AF?

A
  • Less effective at controlling HR during exercise
  • Only considered if the person does no or very little physical exercise or other rate-limited drug
  • May have a role in co-existent HF
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62
Q

What medications are considered in Rhythm Control?

A

Beta blockers
Dronedarone: Second-line in patients following cardioversion
Amiodarone: particularly if co-existing heart failure

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63
Q

How long should a patient be anticoagulated before catheter ablation?

A
  • Should be used 4 weeks before and during the procedure

- Does not reduce stroke risk - must be anti-coagulated via CHADs-VASc

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64
Q

For catheter ablation, on the CHADsVASc score - if a patient scores 0 how long must they be anti-coagulated for?

A

2 months

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65
Q

For catheter ablation on the CHADsVASc score - if a patient scores >1 how long must they be anticoagulated for?

A

Long-term

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66
Q

What are the complications of a catheter ablations?

A

Cardiac Tamponade
Stroke
Pulmonary Vein Stenosis

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67
Q

What is the success rate for a catheter ablation?

A

50% of patient experience an early recurrence of AF that resolves spontaneously

55% of patients with the single procedure remain in sinus rhythm. For multiple procedures 80% are in sinus rhythm.

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68
Q

What are the main characteristics of lung cancer?

A

Haemoptysis
History of smoking
Anorexia, weight loss

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69
Q

What are some of the causes of haemoptysis?

A 
Lung cancer
Pulmonary oedema 
Tuberculosis
PE 
LRTI
Bronchiectasis 
Mitral Stenosis 
Aspergilloma
Granulomatosis with Polyangiitis
Goodpasture's
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70
Q

What are the main characteristics of pulmonary oedema?

A

Haemoptysis
Dyspnoea
Bibasal crackles and S3 are most reliable signs

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71
Q

What are the main characteristics of tuberculosis?

A 
Fever
Night sweats 
Anorexia 
Weight loss
Haemoptysis
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72
Q

What are the main characteristics of PE?

A

Pleuritic Chest Pain
Tachycardia
Tachypnoea
Haemoptysis

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73
Q

What are the main characteristics of LRTI?

A

History of purulent cough

Haemoptysis

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74
Q

What are the main characteristics of bronchiectasis?

A

Usually long history of cough and daily purulent sputum production
Haemoptysis

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75
Q

What are the main characteristics of Mitral Stenosis?

A

Haemoptysis
Atrial Fibrillation
Malar Flush on Cheeks
Mid-diastolic murmur

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76
Q

What are the main characteristics of aspergilloma?

A

History of TB
Haemoptysis
Chest Xray shows Rounded Opacity

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77
Q

What are the main characteristics of Granulomatosis with polyangiitis?

A

Upper respiratory tract - Epistaxis, sinusitis, nasal crusting

Lower respiratory tract: Dyspnoea, haemoptysis
Glomerulonephritis
Saddle Shaped nose deformity

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78
Q

What are the main characteristics of Goodpastures?

A

Haemoptysis
Systemically unwell: fever, nausea
Glomerulonephritis

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79
Q

What are the genetics of Tuberous Sclerosis?

A

Autosomal Dominant

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80
Q

What are the cutaneous features of Neurofibromatosis?

A
  • Depigmented ‘ash-leaf’ spots which fluoresce under UV light
  • Rough patches of skin over lumber spin (Shagreen Patches)
  • Adenoma sebaceum (angiofibromas) - butterfly over nose
  • Fibromata beneath nails (Subungual fibromata)
  • Cafe au lait spots
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81
Q

What are the roughened patches of skin over lumbar spine in Tubular Sclerosis called?

A

Shagreen Patches

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82
Q

What is the butterfly distribution over nose in Tubular sclerosis called?

A

Adenoma sebaceum (angiofibroma)

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83
Q

What are the neurological features of TS?

A

Developmental delay
Epilepsy (infantile spasms or partial)
Intellectual impairment

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84
Q

What are the features of TS in the eyes?

A

Retinal hamartomas - white areas on retina

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85
Q

What are the heart features of TS?

A

Rhabdomyomas of the heart

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86
Q

What are the brain features in TS?

A

Gliomatous changes in brain lesions

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87
Q

What are the renal features of TS?

A

PC Kidneys, renal angiomyolipomata

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88
Q

What are the lung features of TS?

A

Lymphangioleiomyomatosis: lung cysts

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89
Q

Summarise the features of TS?

A

Ash-leaf spots
Adenoma Sebaceum
Shagreen Patches
Subungual fibromata

Epilepsy
Developmental problems
Retinal hamartomas

Neurocutaneous disorders
Autosomal dominant
Ocular haemartomas

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90
Q

What are the main features of Neurofibromatosis?

A

Axillary/groin freckles
Phaeochromocytomas
NF2 - acoustic neuroma and other CNS tumours

Iris hamartomas
Neurocutaneous disorders
Autosomal dominant
Ocular Haemartomas

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91
Q

What is the pathophysiology of DKA?

A
  • Uncontrolled lipolysis (not proteolysis) which results in an excess of free fatty acids that are ultimately converted to ketone bodies.
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92
Q

What are the features of DKA?

A 
Abdominal pain 
Polyuria
Polydipsia
Dehydration 
Kussmaul Respiration 
Acetone-smelling breath
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93
Q

What is the diagnostic criteria for DKA?

A

Glucose >11 or known DM
pH <7.3
Bicarb <15
Ketones >3 mmols or urine ketones ++ on dipstick

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94
Q

What are the 4 principles of management for DKA?

A
  • Fluid replacement
  • Insulin
  • Correction of electrolyte disturbance

– Long acting insulin should be continued, short-acting insulin should be stopped

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95
Q

What intravenous infusion of insulin should be started for DKA?

A
  • 0.1unit/kg/hour

- Once blood glucose is <15 an infusion of 5% dextrose should be started

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96
Q

What is the reasoning behind replacing potassium in DKA?

A
  • Serum K is high on admission despite low K in the body

This often falls following insulin treatment resulting in hypokalaemia

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97
Q

What is the definition of resolution of DKA?

A

pH >7.3
Blood Ketones <0.6
Bicarbonate >15

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98
Q

What should happen once DKA has resolved?

A
  • Ketonaemia + acidosis should resolve in 24hrs - if not patient requires senior review from endocrinologist
  • If above criteria are met patient is eating and drinking switch to subcut insulin
  • Patient should be reviewed by DSN prior to discharge
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99
Q

What are the complications of DKA?

A
  • Gastric Stasis
  • Thromboembolism
  • Arrythmias 2ndry to HyperK or low K
  • Iatrogenic due to incorrect fluid therapy - cerebral oedema, hypokalaemia, hypoglycaemia
  • Acute respiratory distress syndrome
  • Acute Kidney Injury
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100
Q

What are the features of pericarditis?

A
  • Chest pain - pleuritic often relieved by sitting forwards
  • Non-productive cough, dyspnoea, flu-like symptoms
  • Pericardial rub
  • Tachypnoea
  • Tachycardia
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101
Q

Causes of a pericarditis?

A 
Coxsackie 
Tuberculosis 
Uraemia (fibrinous pericarditis) 
Trauma 
Post MI - Dressler's 
Connective tissue disease 
Hypothyroidism 
Malignancy
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102
Q

What are the ECG findings in pericarditis?

A

ECG - change in pericarditis are often global/widespread not territories seen in ischaemic events

  • Saddle-shaped ST elevation
  • PR depression: most specific ECG marker
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103
Q

What is the most specific ECG marker for pericarditis?

A

PR Depression

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104
Q

What is the management for pericarditis?

A

Combinations of NSAIDs and Colchicine first line for patients with acute idiopathic or viral pericarditis

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105
Q

What is De Quervain’s Thyroiditis?

A

Subacute Thyroiditis (De Quervain’s Thyroiditis) occurs following a viral infection and typically presents with hyperthyroidism

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106
Q

How many phases of Quervain’s Thyroiditis are there?

A

4

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107
Q

What is the first phase of De Quervain’s Thyroiditis and how long does it last?

A

Phase 1 - Last 3-6 weeks with hyperthyroidism, painful goitre and raised ESR

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108
Q

What is phase 2 of De Quervain’s Thyroiditis and how long does it last?

A

Phase 2 - Euthyroid for 1-3 weeks

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109
Q

What is phase 3 of De Quervain’s Thyroiditis and how long does it last?

A

Phase 3 (weeks - months) - Hypothyroidism

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110
Q

What is phase 4 of De Quervain’s Thyroiditis and how long does it last?

A

Phase 4 - thyroid structure and function goes back to normal

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111
Q

What is the key investigation for Subacute De Quervain’s Thyroiditis?

A

Thyroid Scintigraphy: Globally reduced uptake of iodine-131

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112
Q

What is the management of Subacute Thyroiditis?

A
  • Self-limiting - most patients do not require treatment
  • Thyroid pain may respond to aspirin or NSAIDs
  • In more severe cases consider steroids - particularly if hypothyroidism develops
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113
Q

What is the main findings in primary hyperthyroidism?

A

Heat intolerance, insomnia, agitation, goitre. Normal TSH and high T4.

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114
Q

What does primary hyperthyroidism mean?

A

Pathology within gland itself rather than hypothalamus/pituitary

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115
Q

What is carbimazole considered for treatment of hyperthyroidism?

A

Graves - not for subacute thyroiditis

Subacute thyroiditis commonly resolves spontaneously - no need to reduce thyroid hormone

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116
Q

When is propylthiouracil considered treatment for chronic hyperthyroidism?

A

Used in Graves - for chronic cause therefore not for subacute thyroiditis

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117
Q

What is Clopidogrel?

A
  • Antiplatelet agent used to treat cardiovascular disease

- Antagonist of the PSY12 ADP receptor - inhibiting the activation of platelets

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118
Q

What class does clopidogrel belong to? Give examples of other members?

A

Thienopyridines

  • Prasugrel, ticagrelor, ticlopidine
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119
Q

What is the presentation of DIC?

A

Oliguria
Hypotension
Tachycardia
Bleeding - Haematuria, petechial bruising and bleeding from cannula

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120
Q

What is the typical blood picture for DIC?

Platelets, fibrinogen, PT and APTT, Fibrinogen Degradation Products?

A

Low PLatelets
Low fibrinogen
Increased PT and APTT
Increased FDP

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121
Q

Summarise the coagulation cascade’s role?

A

Coagulation cascade –> thrombin.
Thrombin converts fibrinogen to fibrin.
Fibrin clot is the final product of haemostasis.

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122
Q

Summarise the fibrinolytic system’s role?

A

Fibrinolytic system breaks down fibrinogen and fibrin.

The activation of the fibrinolytic system makes plasmin (in the presence of thrombin) which breaks down fibrin clots.

The breakdown of fibrinogen and fibrin produces fibrin degradation products.

The presence of plasmin is important as the central proteolytic enzyme of coagulation and also fibrinolysis.

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123
Q

Describe the crucial mediator in DIC?

A

Tissue Factor

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124
Q

What is tissue factor?

A

Present on surface of cells and not normally in contact with general circulation.

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125
Q

How does TF trigger DIC?

A

Exposed when vascular damage occurs. It is release in response to exposure to cytokines (IL1, TNF, Endotoxin).

TF binds to coagulation factors that then triggers the extrinsic pathway via F8. This triggers the intrinsic pathway of coagulation.

What are the two hallmarks of DIC - Generation of Fibrin and consumption of procoagulants.

Without functional counteraction from the anticoagulant pathways - Increased thrombin amplifies coagulation cascade through +ve feedback.

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126
Q

What are the causes of DIC?

A

Sepsis
Trauma
Obstetric complications (amniotic fluid embolism, increased LFTs, Low platelets (HELLP)
Malignancy (haematological and solid malignancy are risk factors for DIC)

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127
Q

What are the clotting findings on warfarin administration

A

PT - prolonged
APTT - Normal
Bleeding time - Normal
Platelets - Normal

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128
Q

What are the clotting findings on aspirin administration

A

PT - Normal
APTT - Normal
Bleeding time - Prolonged
Platelet - Normal

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129
Q

What are the clotting findings on heparin administration

A

PT - Normal (can be prolonged)
APTT - prolonged
Bleeding time - Normal
Platelets - Normal

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130
Q

What are the clotting findings on DIC?

A

PT - Prolonged
APTT - prolonged
Bleeding time - Prolonged
Platelets - Low

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131
Q

What is the most commonly affected site for necrotising fasciitis?

A

Perineum (Fournier’s Gangrene)

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132
Q

What are the features of necrotising fasciitis?

A
  • Acute Onset
  • Pain, swelling, erythema at site
  • Often with rapidly worsening cellulitis with pain out of keeping with physical features
  • Tender over infected issues with hypoaesthesia to light touch
  • Fever/Tachycardia later
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133
Q

What is the management of necrotising fasciitis?

A

Surgical debridement

IV Abx

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134
Q

Patient with severe pain in perineum + scrotum, T2DM with dapagliflozin w/ purple rash bullae with intense pain. Tachy with temperature.

A

Necrotizing fasciitis (Fournier’s Gangrene)

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135
Q

What is type 1 necrotising fasciitis?

A

Type 1 - Mixed anaerobes and aerobes - most common

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136
Q

What is type 2 necrotising fasciitis?

A

Type 2 - Streptococcus Pyogenes

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137
Q

What are the risk factors for necrotising fasciitis?

A

Skin factors: recent trauma, burns or soft tissue infections
DM - Most common (SGLT02 Inhibitor important cause)
IV Drug use
Immunosuppression

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138
Q

What helps distinguish necrotising fasciitis from cellulitis?

A

Bullae in rash, purple discolouration, severe pain with additional risk factors.

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139
Q

What is pyoderma gangrenosum?

A

Rapidly enlarging, painful ulcer associated with IBD and rheumatoid arthritis

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140
Q

What is Hidradenitis suppurativa?

A

Chronic inflammatory skin disease leading to inflammatory lesions, pustules, abscesses in groin area. Lesions are painful but arise slowly.

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141
Q

What is a GCS Motor 6?

A

Obeys commands

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142
Q

What is a GCS Motor 5?

A

Localises to pain

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143
Q

What is GCS motor 4?

A

Withdraws from pain

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144
Q

What is GCS motor 3?

A

Abnormal flexion to pain

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145
Q

What is GCS Motor 2?

A

Extending to pain

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146
Q

What is GCS Motor 1?

A

None

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147
Q

What is GCS Verbal 5?

A

Orientated

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148
Q

What is GCS Verbal 4?

A

Confused

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149
Q

What is GCS Verbal 3

A

Words

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150
Q

What is GCS Verbal 2?

A

Sounds

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151
Q

What is GCS Verbal 1?

A

None

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152
Q

What is GCS Eyes 4?

A

Spontaneous

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153
Q

What is GCS Eyes 3?

A

To speech

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154
Q

What is GCS Eyes 2?

A

Pain

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155
Q

What is GCS Eyes 1?

A

None

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156
Q

What is the diagnostic criteria for diabetes if they are symptomatic?

A

Diagnosis = plasma glucose of HbA1c. Depends if symptomatic or not.

If symptomatic - single abnormal HbA1c >48 or fasting plasma of >7 or random glucose greater than 11.1

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157
Q

What is the diagnostic criteria for diabetes if asymptomatic?

A

If asymptomatic - not diagnosed on a single abnormal HbA1c or plasma glucose. Repeat testing (ideally same test).

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158
Q

What does a HbA1c of <48 mean?

A

Does not exclude diabetes (it is not sensitive as fasting samples for detecting diabetes.

In patients without symptoms the test must be repeated to confirm diagnosis.

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159
Q

What is the definition of pre-diabetes?

A

Individual at risk of developing T2DM

  • HbA1c 42-47
  • Fasting plasma glucose 6-9

use a risk-assessment tool to identify those at risk of T2DM
- Offer lifestyle adjustment

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160
Q

Which conditions would HbA1c not be used for?

A
  • Haemoglobinopathies
  • Haemolytic anaemia
  • Untreated iron deficiency anaemia
  • Suspected Gestational Diabetes
  • Children
  • HIV
  • CKD
  • Taking steroids (induce hyperglycaemia)
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161
Q

What is the definition of impaired fasting glucose?

A

A fasting glucose >= 6.1 but less than 7

People with IFG should be offered OGTT to rule out diagnosis of diabetes. Result <11.1 but above 7.8 indicates IGt

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162
Q

What is the definition of impaired glucose tolerance?

A

Fasting glucose <7 and OGTT 2hr value >= 7.8 but less than 11.1

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163
Q

What does HSV-1 account for?

A

Oral lesions (cold sore) - there is now considerable overlap.

Commonly triggers by sunlight (following a holiday)

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164
Q

What does HSV-2 account for?

A

Genital herpes (considerable overlap) - painful genital ulceration

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165
Q

What is the management for herpes gingivostomatitis?

A

Oral aciclovir, chlorhexidine mouthwash

166
Q

What is the management for cold sores?

A

Topical aciclovir

167
Q

What is the management for genital herpes?

A

Oral aciclovir - with more frequent exacerbations

168
Q

What is advised is an attack of herpes occurs during pregnancy?

A

Elective caesarean if primary attack occurs >28 weeks gestation

169
Q

What is advised regarding pregnancy for a women with recurrent herpes?

A

Advised to be treated with suppressive therapy and advised risk of transmission to baby is low

170
Q

What is the definition of traveller’s diarrhoea?

A

> =3 loose watery stools in 24hrs with or without abdominal cramps, fever, vomiting or blood in the stool.

171
Q

What is the most common cause of traveller’s diarrhoea?

A

E.coli

172
Q

What is the pattern of illness of acute food poisoning?

A

Sudden onset vomiting, nausea, diarrhoea after ingestion of toxin.

Caused by Staph A, B Cereus, Clostridium Perfringens

173
Q

Which bacterias cause diarrhoea within 1-6hrs?

A 
Staph A 
Bacillus Cereus (vomiting subtype - diarrhoeal illness has incubation of 6-14hrs)
174
Q

Which bacterias have an incubation time of 12-48hrs?

A

Salmonella

E.coli

175
Q

Which bacterias have an incubation time of 48-72hrs?

A

Shigella

Campylobacter

176
Q

Which bacteria has an incubation time of >7 days?

A

Giardiasis

Amoebiasis

177
Q

What are the features of E.coli diarrhoea?

A
  • Watery stools
  • Common amongst travellers
  • Abdominal cramps and nausea
178
Q

What are the features of giardiasis diarrhoea?

A

Prolonged non-bloody diarrhoea

179
Q

What are the features of cholera diarrhoea?

A

Profuse watery diarrhoea
Severe dehydration resulting in weight loss
Not common amongst travellers

180
Q

What are the features of shigella diarrhoea?

A

Bloody diarrhoea

Vomiting and abdominal pain

181
Q

What are the features of staph a diarrhoea?

A

Severe vomiting

Short incubation period

182
Q

What are the features of camylobacter diarrhoea?

A

Flu-like prodrome
Crampy abdominal pain, fever, diarrhoea (can be bloody)
May mimic appendicitis
Complications include GBS

183
Q

What are the features of B cereus diarrhoea?

A

Two types

  • 1) Vomiting in 6hrs - due to rice
  • 2) Diarrhoeal illness occuring after 6 hrs
184
Q

What are the features of amoebiasis diarrhoea?

A

Gradual onset bloody diarrhoea, abdominal pain and tenderness which may last several weeks.

185
Q

If someone is on Morphine oral 60mg BD how do you convert this to subcut?

A

Subcut/IM or IV is equivalent to half of oral dose.

60mg IV.

186
Q

28yr old with SOB, abdo discomfort, dry cough, widespread skin rash with erythema multiforme, hyponatraemia?

A

Mycoplasma Pneumoniae Pneumonia

187
Q

What are the features of a MYcoplasma Pneumonia?

A
  • Prolonged + gradual onset
  • Flu-like symptoms classically precede a dry cough
  • Bilateral consolidation on X-ray
188
Q

What are some complications of mycoplasma pneumonia?

A
  • Cold agglutins - IgM - may cause a haemolytic anaemia, thrombocytopenia.
  • Erythema multiforme or erythema nodosum
  • Meningoencephalitis, GBS
  • Bullous Myringitis - painful vesicles on tympanic membrane
  • Pericarditis/myocarditis
  • Gastrointestinal: hepatitis/pancreatitis
  • Acute glomerulonephritis
189
Q

How often to epidemics of mycoplasma pneumoniae occur?

A

Every 4 years

190
Q

What are the investigations of Mycoplasma pneumoniae?

A

Mycoplasma serology

Positive Cold Agglutination Test

191
Q

What is the management of mycoplasma pneumoniae?

A

Doxycycline

Macroline (erythromycin/clarithromycin)

192
Q

What are the features of staphylococcal pneumonia?

A
  • May complicate influenza infection
  • Most frequently in elderly and in IV drug users or those with underlying disease.
  • Can cause a a caveating pneumonia
193
Q

What are the features of a pneumocystis jiroveci pneumonia?

A

Immunocompromised patients - presents with exertional breathlessness and patients seen with desaturate on walking.
- HIV test

194
Q

What are the features of a legionella pneumonia?

A 
Lymphopenia 
Hyponatraemia 
Diagnosed with urinary antigen 
Atypical pneumonia 
Flu like symptoms 
Dry cough 
Deranged LFT 
Treat with macrolide
195
Q

What are the features of pericarditis on ECG?

A

PR depression
Widespread ST elevation
Reciprocal ST depression and PR elevation in aVR and V1

196
Q

Which infants is the BCG recommended to?

A

All infants (0-12m) living in areas of UK with annual incidence of TB is 40/100,000 or greater

All infants (0-12m) with a parent or grandparent who is born in a country where annual incidence of TB is 40/100,000 or greater. This applies to older children but if they are >6yrs they need a tuberculin skin test

197
Q

Which work personnel are required to have BCG vaccine?

A

Under age of 35 and

  • Healthcare workers
  • Prison Staff
  • Staff of care home for the elderly
  • Those who work with homeless people
198
Q

Which group of exposed individuals require BCG vaccine?

A
  • Previously unvaccinated tuberculin-negative contacts of cases of resp TB
  • Previously unvaccinated, tuberculin-negative new entrants under 16 yrs of age who were born in or who have lived for prolonged period (3 months) in a country with an annual TB incidence of 40/100,000.
199
Q

What are the contraindications for BCG?

A
  • Previous BCG Vaccination
  • A past history of TB
  • HIV
  • Pregnancy
  • Positive Tuberculin Test (heaf or Mantoux)
200
Q

What is the management of Addison’s Disease?

A

Glucocorticoid and Mineralocorticoid replacement therapy

  • Hydrocortisone: usually given in 2 or 3 divided doses. Patients typically require 20-30mg per day, with majority given in the first half of day.
  • Fludrocortisone
201
Q

What is important to emphasise to Addison’s Disease patients regarding management?

A
  • Emphasise importance of not missing glucocorticoid
  • Consider MedicAlert Bracelets and Steroid Cards
  • Patients should be provided with hydrocortisone for injection with needles and syringes to treat an adrenal crisis
  • Discuss how to adjust the glucocorticoid dose during an intercurrent illness.
202
Q

How do you manage an intercurrent illness during an Addisonian Crisis?

A
  • Glucocorticoid dose should be doubled with fludrocortisone dose staying the same
  • Review Addison’s Clinical Advisory Panel.
203
Q

What is the most common anaemia worldwide?

A

IDA

204
Q

Which age group has the highest prevalence of IDA?

A

Preschool-age children

205
Q

How does IDA lead to an anaemia?

A

Iron needed to make Hb therefore low iron leads to reduction in RBC.

206
Q

What are the main causes of IDA?

A
  • Excessive blood loss
  • Inadequate dietary intake
  • Poor intestinal absorption
  • Increased Iron Requirement
207
Q

How does excessive blood loss occur to cause IDA?

A
  • Menorrhagia (most common in pre-menopausal women)

- GI Bleeding in men (?colon cancer) and post-menopausal women

208
Q

How does inadequate dietary intake cause IDA?

A

Meat is a good source of iron - vegans + vegetarians more likely to develop IDA due to lack of meat. Dark green, leafy vegetables can contribute.

209
Q

How does poor intestinal absorption cause IDA?

A

Small intestine pathology - Coeliacs

210
Q

How does increased iron requirements cause IDA?

A

Children have increased Iron requirements - during periods of growth.
Women during pregnancy
due to foetus and increased plasma volume.

211
Q

What are the features of IDA?

A 
Fatigue
SOB on exertion 
Palpitations 
Pallor
Nail changes - koilonychia 
Hair loss
Atrophic glossitis 
Post-cricoid webs 
Angular stomatitis
212
Q

What investigations are required for IDA?

A

History
Bloods - Hypochromic, microcytic anaemia
Blood film
Endoscopy to rule out malignancy +/- Gastro referral

213
Q

What are the findings on bloods for IDA and why?

A

Serum Ferritin = low (correlates with iron store)
TIBC (total iron-binding capacity)/transferrin = High reflecting low iron stores.

Transferrin saturation is low (percentage of tranferrin proteins saturated with iron)

214
Q

What is the management of IDA?

A

IDA underlying cause found

  • Oral ferrous sulphate for 3 months after iron deficiency has been corrected
  • Iron rich diet
215
Q

What are common diet effects of iron supplementation?

A

Nausea
Abdominal pain
Constipation
Diarrhoea

216
Q

What is the gold standard investigation for diagnosing degenerative cervical myelopathy?

A

MRI Cervical Spine

217
Q

What is revealed on MRI for Degenerative Cervical Myelopathy?

A

Disc degeneration and ligament hypertrophy with accompanying cord signal change

218
Q

What are the risk factors associated with degenerative cervical myelopathy?

A

Smoking (effect on intervertebral disc)
Genetics
Occupation - Those with high axial loading

219
Q

What are the symptoms of DCM?

A
  • Pain (neck, upper or lower limbs)
  • Loss of motor function (loss of digital dexterity, preventing simple tasks like holding a fork or doing shirt, buttons, arm or leg weakness leading to impaired gait and imbalance
  • Loss of sensory functions causing numbness
  • Loss of autonomic function (urinary and faecal incontinence) -
  • Hoffman’s sign - gently flicking one finger on a patient’s hand. Reflex twitching of the other finger on the same hand in response to the flick
220
Q

Management of patients with DCM?

A
  • Urgent referral for specialist spinal services - neurosurg or orthopaedics
  • Due to importance of treatment

Decompressive surgery is only effective treatment to prevent disease progression
Caution about physiotherapy regarding manipulating spinal cord damage

221
Q

58yr old Patient presenting with 1yr history of worsening erythematous rash, forehead and cheeks with telangiectasia and papules. Rash aggravated by sun and hot/spicy food. What is the rash?

A

Acne Rosacea

222
Q

What are the typical signs/symptoms of acne rosacea?

A 
Affects nose, cheek, forehead
Flushing of skin first symptoms 
Telangiectasia are common
Later develops persistent erythema with papules and pustules
Rhinophyma 
Ocular involvement: blepharitis 
Sunlight may exacerbate symptoms
223
Q

What is the first line management for Acne Rosacea MIld?

A

Topical Metronidazole for Mild (Limited number of papules, pustules, no plaques).

224
Q

In rosacea what can be considered for patients with predominantly flushing symptoms with limited telangiectasia?

A

Brimonidine topical

225
Q

What is the management of severe acne rosacea?

A

Oral Doxycycline (tetracyclines - oxytetracycline)

226
Q

Give examples of Tricyclic antidepressants?

A 
Amitriptyline 
Clomipramine 
Imipramine 
Dosulepin
Trazodone
Lofepramine
Nortriptyline
227
Q

What are Tricyclics used for?

A

Used in Depression (less common due to side-effects and toxicity)
Used for neuropathic pain - smaller doses)

228
Q

What is the MOA of tricyclics?

A

Block reuptake of serotonin and norepinephrine in presynaptic terminals

Antimuscarinic are a subtype of anticholinergic.

229
Q

What are the side-effects of tricyclics?

A

Antimuscarinic side-effects

  • Drowsiness
  • Dry mouth
  • Blurred vision
  • Constipation
  • Urinary Retention
  • Lengthening of QT
230
Q

What does the combined test for Down’s Syndrome consist of?

A

Nuchal Translucency 12 weeks

Blood test for B-HCG and PAPP-A

231
Q

What is the combined test performed?

A

11 and 13+6 weeks

232
Q

What results from the combined test indicate an increased chance of Down’s Syndrome?

A

Nuchal translucency increased
B-HCG raised
PAPP-A low

233
Q

What test is available to women too late for the combined test?

A

The triple or Quadruple test.
Triple: Alpha-fetoprotein, unconjugated oestriol, human chorionic gonadotrophin
Quadruple: Alpha-fetoprotein, unconjugated oestriol, human chorionic gonadotrophin and inhibin A

234
Q

What does the triple test consist of? and when

A

triple test: alpha-fetoprotein, unconjugated oestriol, human chorionic gonadotrophin
At 15-20 weeks

235
Q

What does the quadruple test consist of? and when?

A

quadruple test: alpha-fetoprotein, unconjugated oestriol, human chorionic gonadotrophin and inhibin-A

At 15-20 weeks

236
Q

Man with previous cervical laminectomy for degenerative cervical myelopathy presents with a 2 month history of worsening gait instability and urinary urgency?

A

Recurrent degenerative cervical myelopathy

237
Q

How does recurrent degenerative cervical myelopathy occur?

A

Postoperatively - patients require ongoing follow-up as pathology can recur at adjacent spinal levels - known as adjacent segment disease.

238
Q

What is the presentation of transverse myelitis?

A

Acute presentation
Sensory level
Upper motor neuron signs below the affect level
Features of optic neuritis

239
Q

Presentation of cauda equina syndrome?

A

Leg weakness
Saddle anaesthesia
Sphincter disturbance

240
Q

What are the risk factors for degenerative cervical myelopathy?

A

Smoking (effect on intervertebral discs, genetics and occupation - high axial loading)

241
Q

Presentation of degenerative cervical myelopathy?

A

Can be subtle - vary in severity day to day.

Pain (neck, upper or lower limbs)
Loss of motor function (loss of digital dexterity, preventing simple tasks such as holding form, arm or leg weakness/stiffness leading to impaired gait or imbalance)
Loss of sensory function causing numbness
Loss of autonomic function (urinary or faecal incontinence)
Hoffman’s sign - flicking one finger on patient’s hand. Positive result shows twitching of the other fingers on the same hand in response

242
Q

What is the gold standard test for DCM?

A

MRI Cervical spine - showing disc degeneration and ligament hypertrophy with cord signal change
- all patient should be urgently referral to ensure permanent cord damage. Decompressive surgery is the only effective treatment.

243
Q

What is Beck’s Triad?

A

Falling BP
Rising JVP
Muffled heart sounds - cardiac tamponade

244
Q

What is Beck’s triad indicative of?

A

Cardiac Tamponade - Hypotension, Raised JVP, Muffled Heart sounds?

245
Q

What are the other signs of cardiac tamponade?

A 
Dyspnoea
Tachycardia
Absent Y descent on the JVP 
Pulsus paradoxus - drop in BP during inspiration 
Kussmaul's sign - debate
246
Q

ECG sign for cardiac tamponade?

A

Electric alternans

247
Q

Difference between Cardiac Tamponade and Constrictive pericarditis in terms of JVP?

A

Cardiac tamponade
- JVP absent Y descent (TAMPONADE = TAMPAX (no Y)
Constictive - X and Y present

248
Q

Difference between Cardiac Tamponade and Constrictive pericarditis in terms of BP?

A

Tamponade - Pulsus paradoxus present

Constrictive Peri - absent

249
Q

Characteristic feature of Constrictive pericarditis on CXR?

A

Pericardial Calcification

250
Q

Patient post PCI has drop in BP, raised JVP and muffled heart sounds? What is the best management?

A

Tamponade - for Pericardiocentesis

Recognised complication of PCI post MI

251
Q

Healthy couple cannot conceive in 4 months? What is the management?

A

Address how couple have intercourse and reassure.
Healthy couple can expect to conceive in one year.

Investigations performed after this. Address any mechanical reason that are preventing couple from conceiving.

252
Q

Basic investigations for lack of conception?

A

Semen analysis

Serum progesterone 7 days prior to expected next period. Day 21

253
Q

Interpretation of serum progestogen? <16nmol?

A

Repeat - if still low refer to specialist

254
Q

Interpretation of serum progestogen? 16-30nmol?

A

Repeat

255
Q

Interpretation of serum progestogen? >30nmol?

A

Indicated ovulation

256
Q

What are the key counselling points for infertility?

A

Folic acid
BMI 20-25
Regular sexual intercourse every 2 to 3 days
Smoking and drinking advice

257
Q

What is presbycusis?

A

Age related sensorineural hearing loss

Audiometry demonstrates bilateral high-frequency hearing loss

258
Q

What is otosclerosis?

A

Autosomal dominant - replacement of normal bone with vascular spongy bone.

Onset 20-40yrs.

259
Q

What are the signs of otosclerosis?

A

Conductive deafness
Tinnitus
Tympanic membrane - 10% have a flamingo tinge - hyperaemia
Positive family history

260
Q

What are the signs of glue ear?

A

Otits media with effusion

  • peaks at 2 years
  • Hearing loss usually a presenting feature (glue ear is commonest cause of conductive hearing loss and elective surgery in childhood
  • Can cause speech and language delay, behavioural or balance problems
261
Q

What is meniere’s - how does it present?

A

Common in middle-aged adults

  • Episodes of vertigo, tinnitus and hearing loss (sensorineural). Vertigo is prominent symptoms.
  • Sensation of aural fullness or pressure
  • Nystagmus and positive romberg’s test
  • Lasting minutes to hours §
262
Q

What can cause drug ototoxicity?

A
  • Aminoglycosides - Gentamicin, furosemide, aspirin, other cytotoxic agents
263
Q

What are the findings of an acoustic neuroma?

A

VIII: hearing loss, vertigo.
VL absent corneal reflex
VII: Facial palsy

Seen in Neurofibromatosis type 2

264
Q

What does Vitamin A (retinoids) deficiency cause?

A

Night-blindness

265
Q

What does Vitamin B1 (thiamine) deficiency cause?

A

Beri-beri

Polyneuropathy, Wernike-Korsakoff Syndrome
Heart failure

266
Q

What does Vitamin B3 (Niacin) deficiency cause?

A

Pellagra

  • Dermatitis
  • Diarrhoea
  • Dementia
267
Q

What does Vitamin B6 (Pyridoxine) deficiency cause?

A

Anaemia
Irritability
Seizures

268
Q

What does Vitamin B7 (Biotin) deficiency causE?

A

Dermatitis

Seborrhoea

269
Q

What does Vitamin B9 (Folic Acid) deficiency cause?

A

Megaloblastic anaemia deficiency during pregnancy- neural tube defects

270
Q

What does Vitamin B12 (Cyanocobalamin) deficiency cause?

A

Megaloblastic anaemia

Peripheral Neuropathy

271
Q

What does Vitamin C (ascorbic acid) deficiency cause?

A

Scurvy

  • Gingivitis
  • Bleeding
272
Q

What does Vitamin D (ergocalciferol, cholecalciferol) deficiency cause?

A

Rickets

Osteomalacia

273
Q

What does Vitamin E Deficiency cause? (Tocopherol, Tocotrienol)

A

Mild haemolytic anaemia in newborn infants
Ataxia
Peripheral neuropathy

274
Q

What does Vit K (Naphthoquinone) defiency cause?

A

Haemorrhagic disease of the newborn, bleeding diathesis

275
Q

What are features of opioid misuse?

A 
Rhinorrhoea
Needle track marks 
Pinpoint pupils 
Drowsiness
Watering eyes
Yawning
276
Q

What are the complications of opioid misuse?

A

Viral infections (sharing needles) - HIV, Hep B/C
Bacterial infections (injecting): Infective endocarditis, septic arthritis, septicaemia, necrotising fasciitis
VTE
Overdose –> respiratory depression
Psychological problems: craving
Social problems: crime, prostitution, homelessness

277
Q

What is the emergency management of an opioid overdose

A

IV or IM Naloxone - rapid onset and short duration of action

278
Q

What is the management of opioid dependence?

A

Managed by specialist drug dependence clinics
May be offered maintenance therapy or detox
NICE recommends methadone or buprenorphine as first line
Compliance monitored using urinalysis
Detox normally lasts 4 weeks in inpatient setting or 12 weeks in community.

279
Q

What type of cytotoxic agent is cyclophosphamide?

A

Alkylating agent - causing cross linking DNA.

280
Q

What are the adverse affects of cyclophosphamide?

A

Haemorrhagic cystitits
Myelosuppression
Transitional cell carcinoma

281
Q

What type of cytotoxic agent is bleomycin?

A

Cytotoxic antibiotic - Degrades preformed DNA.

282
Q

What are the adverse affects of Bleomycin?

A

Lung Fibrosis

283
Q

What type of cytotoxic agent is Anthracyclines (doxyrubicin)?

A

Cytotoxic antibiotics

  • Stablises DNA-topoisomerase II complex
  • Inhibits DNA and RNA Synthesis
284
Q

What are the adverse affects of anthracyclines?

A

Cardiomyopathy

285
Q

What type of cytotoxic agent is methotrexate?

A

Antimetabolite

- Inhibits dihydrofolate reductase and thymidylate synethesis

286
Q

What are the adverse effects of methotrexte?

A

Myelosuppression
Mucositis
Liver fibrosis
Lung fibrosis

287
Q

What type of cytotoxic agent is Fluorouracil (5-FU)

A

Pyrimidine analogue inducing cell cycle arrest and apoptosis by blocking thymidylate synthase

288
Q

What are the adverse effects of 5-FU?

A

Myelosuppression
Mucositis
Dermatitis

289
Q

What type of cytotoxic drug is 6-mercaptopurine?

A

Antimetabolite

Pure analogue that is activated by HGPRTase, decreasing purine synthesis

290
Q

What are the adverse effects of 6-mercaptopurine?

A

Myelosuppression

291
Q

What type of cytotoxic drug is cytarabine?

A

An antimetabolic

Pyrimidine antagonist - interferes with DNA synthesis

292
Q

What are the adverser effects of cytarabine?

A

Myelosuppression

Ataxia

293
Q

What type of cytotoxic drug is vincristine?

A

Acts on Microtubules

- Inhibits formation of microtubules

294
Q

What are the sideeffects of vincristine?

A

Peripheral neuropathy
Paralytic ileus
(Vinbastine - Myelosuppression)

295
Q

What type of cytotoxic drug is docetaxel?

A

Acts on Microtubules - prevents microtubules depolymerisation and disassemly, decreasing free tubulin

296
Q

What are the adverse effects of docetaxel?

A

Neutropaenia

297
Q

What type of cytotoxic drug is irinotecan?

A

Topoisomerase inhibitor - inhibits topoisomerase 1 which prevents relaxation of supercoiled DNA

298
Q

What are the adverse effects of irinotecan?

A

Myelosuppression

299
Q

What is the MOA of cisplatin?

A

Causes cross-linking in DNA

300
Q

What are the adverse effects of cisplatin?

A

Otoxicity
Peripheral Neuropathy
Hypomagnesaemia

301
Q

What is the MOA of Hydroxyurea?

A

Inhibits ribonucleotide reductase, decreasing DNA synethesis

302
Q

What are the adverse effects of hydroxyurea?

A

Myelosuppression

303
Q

Patient with epistaxis for 20 mins and not responding to pinching nose firmly for 20 mins. NO bleeding point visualised? Next step

A

Anterior packing

- most suitable management for epistaxis where the site is difficult to localise.

304
Q

Is there is a bleeding point visible in epistaxis what management is appropriate?

A

Cautery

305
Q

What are the two types of anterior packing?

A

Dissolvable

Non-dissolvable (rapid rhino - inflatable nasal balloon catheter) and Merocel (absorbent sponge tampon)

306
Q

What should be the next step of management if bleeding continues after anterior packing?

A

Likely posterior bleed - needs referral to ENT for posterior packing

307
Q

What are the sources of bleeding in epistaxis?

A

Anterior bleed - insult to network of capillaries that form Kiesselbach’s plexus

Posterior haemorrhage - more profuse and from deeper structures in elderly patients - risk of airway compromise

308
Q

What are the causes of epistaxis?

A

Most are benign - nose picking/blowing
Trauma to nose
Insertion of foreign bodies
Bleeding disorders - immune thrombocytopenia/Waldenstronm’s Macroglobulinaemia
Juvenile Angiofibroma - benign tumour that is highly vasculised
Cocaine use - nasal septum may be abraded or atrophined (vasoconstrictor leading to obliteration of septum)
Hereditary haemorrhagic telangiectasia
Granulomatosis with polyangiitis

309
Q

What is the first step management of epistaxis?

A

If haemodynamically stable

  • Ask patient to sit with torso forward and mouth open.
  • Pinch cartilaginous area of nose firmly for 20 mins
310
Q

What is the next step if first aid measures are successful?

A

Topical antiseptic such as naseptin (Chlorhexidine and neomycin)
Advise re: risk-factors of rebleed
- If comorbidities consider admission

311
Q

What is the second step in epistaxis is first aid measures fail?

A

If bleeding does not stop for 15 mins -

  • Consider cautery if source of bleed visible with silver nitrate stick
  • Then apply naseptin or muciprocin
312
Q

What is the second step in epistaxis if a bleed source cannot be visualised?

A

Packing -

  • use local anaesthetic spray
  • Pack with head forward
  • Pressure on cartilage
  • Examine patient’s mouth and throat
313
Q

What is the management of a patient who is haemodynamically unstable or compromised with epistaxis

A
  • Control bleeding with first aid measures

- Admit to hospital

314
Q

What is the last step of management if all else failed

A

Sphenopalatine Ligation in Theatre

315
Q

50yr old has a cervical smear 12 months prior showing high risk HPV. A repeat has come back negative for high-risk HPV.

A

Cervical cancer: if 1st repeat smear at 12 months is now hrHPV-ve –> Return to routine recall

316
Q

NHS has now moved to a HPV first system?

A

A sample is tested for high risk strains of HPV first and cytological examination only if this is positive

317
Q

What is the management of a negative hrHPV result?

A

Return to normal recall unles

  • test of cure pathway (individuals treated with CIN1, CIN2, CIN3 should be invited6 months after treatment for a test of cure repeat cervical sample)
  • Untreated CIN1 pathway
  • F/up for incompletely excised cervical glandular intraepithelial neoplasia (CGIN)/stratified mucin producing intraepithelial lesion (SMILE) or cervical cancer
  • Follow-up for boderline changes in endocervical cells
318
Q

What’s the management of a positive hrHPV test?

A

Sample sent to cytology
- If cytology is abnormal –> go to colposcopy

Abnormal cytology - Borderline changes in squamous or endocervical cells 
Low grade dyskaryosis 
High-grade dyskaryosis (Moderate) 
high-grade dyskaryosis 
Invasive squamous cell carcinoma 
Glandular neoplasia
319
Q

What is the management if cytology is normal after hrHPV +ve

A

Test repeated at 12 months
- If repeat test is negative –> Return to normal recall

  • If repeat tet is sitl hrHPV +ve and cytology still normal –> further repeat test 12 months later:
    if hrHPV -ve at 24 months - return to normal recall
    if hrHPV +ve at 24 months –> colposcopy
320
Q

What is routine recall for cervical smear?

A 
25-49 = 3 years
50-65 = 5 years
321
Q

What is the treatment of CIN?

A

LLETZ (large loop excision of transformation zone)

322
Q

BPPV which test is Diagnositic?

A

Dix-hallpike

323
Q

BPPV which test is for treatment?

A

Epley

324
Q

What is BPPV?

A

Canalithiasis (Calcium debris) in semicircular canal leads to endolymph improper motion).

325
Q

What medication is used to treated BPPV?

A

Betahistine (if patient unsuitable for canalith repositioning manoeuvres).

326
Q

What is the dose of adrenaline in anaphylaxis- adult?

A

IM Adrenaline - 0.5ml of 1 in 1,000. Can be repeated every 5 minutes if necessary.

327
Q

What is the dose of adrenaline in anaphylaxis? <6 months?

A

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

328
Q

What is the dose of adrenaline in anaphylaxis? 6 months - 6 years

A

150 micrograms (0.15ml 1 in 1,000)

329
Q

What is the dose of adrenaline in anaphylaxis 6-12 years

A

300 micrograms (0.3ml in 1 in 1,000)

330
Q

How often can adrenaline be repeated?

A

every 5 mins

331
Q

What is refractory anaphylaxis?

A

Respiratory and/or cardiovascular problems despite 2 doses of IM Adrenaline
IV Fluids for shock

332
Q

What is post-stabilisation management of anaphylaxis?

A

non-sedating oral antihistamines
Serum Tryptase
Referral to specialist allergy clinic
Adrenaline injector in interim

333
Q

Which vaccine would be given to an 18yr old about to go to university?

A

Meningitis ACWY. All students in year 9-10 get it.

Catch-up program for students starting uni.

334
Q

19yr old with 10 week gestation presents with intermittent vaginal bleeding over previous months and hyperemesis. Examination reveals a non-tender, large for dates uterus.

A

Molar Pregnancy

  • Form of gestational trophoblastic disease (all genetic material from father).
  • Presents with vaginal bleeding, large for date uterine size and hyperemesis, hyperthyroidism from high volumes of beta-hCG.(hCG can mimic TSH)
335
Q

What is the spectrum of gestational trophoblastic disorders?

A

Complete hydatidiform mole
Partial hydatidiform mole
Choriocarcinoma

336
Q

What is the management of complete hydatidiform mole?

A

Urgent referral to specialist centre

Effective contraception recommended to avoid pregnancy in the next 12 months

337
Q

What is a partial mole?

A

Normal haploid egg fertilised with 2 sperm or 1 sperm with double the chromosomes. DNA is maternal and paternal
in origin.

338
Q

In ALS - if IV Access cannot be achieved how are drugs given?

A

Intraosseous route

339
Q

What are the shockable rhythms in ALS?

A

Ventricular fibrillation

Pulseless ventricular tachycardia (VF/Pulseless VT)

340
Q

What are the non-shockable rhythms?

A

Asystole

Pulseless-electrical activity (Asystole/PEA)

341
Q

When is adrenaline given in ALS?

A

adrenaline 1mg as soon as possible for non-shockable rhythms
During VF/VT cardiac arrest adrenaline 1mg gvein once chest compressions have restarted after the third shock.
Repeat adrenaline 1mg every 3-5 mins whilst ALS continues.

342
Q

When is amiodarone given in ALS?

A

300mg amiodarone given to patients who are VF/Pulseless VT after 3 shocks have been administered.
- A further dose of amiodarone 150mg given to patients who are in VF/Pulseless VT after 5 shocks have been administered

343
Q

What are the 4 Hs?

A

Hypoxia
Hypovolaemia
Hyperkalaemia/hypokalaemia, hypoglycaemia, hypocalcaemia
Hypothermia

344
Q

What are the 4 Ts?

A

Thrombosis
Tension Pneumothorax
Tamponade
Toxins

345
Q

74yr old with left-sided hearing loss with no aural discharge or otalgia with middle ear effusion?

A

Refer to ENT as a 2ww

  • Unilateral glue ear in an adult needs evaluation for a posterior nasal space tumour
  • Tumours can obstruct the opening of the eustachian tubes - leading to persistent middle ear effusion.
346
Q

23yr old with heavy menstrual bleeding over past 3 years. Does not use contraception. Bloods unremarkable.

A

Dysfunctional uterine bleeding

347
Q 
15yr old with menorrhagia - heaving bleeding since menarche. 
Hb 99
Plt 166
PT 13
APTT 49
Bleeding time 15
A

Von Willebrands Disease

  • Most common inherited bleeding disorder.
  • Behave like a platelet disorder - epistaxis and menorrhagia are common whilst haemoarthroses and muscle haematomas are rare.
  • Prolonged bleeding time
    APTT prolonged
    Factor VIII levels may be reduced
    Defective platelet aggregation
348
Q

52 yr old with dyspepsia, dysphagia and fatigue. Long history of dark brown stools, no fresh blood. No unexpected weight loss. Peptic ulcer 10 yrs ago. +ve fro H.pylori.

A

?UGI Cancer - Urgent 2ww referral due to dysphagia. ?chronic Upper GI bleed.

349
Q

What symptoms with dyspepsia warrant urgent 2ww referral?

A

Dysphagia
Upper abdominal mass with stomach cancer
Patients ages ?55 who’s got weight loss and any of the following
- Upper abdo pain
- reflex
- Dyspepsia

350
Q

What are the non-urgent referrals for dyspepsia?

A

Haematemesis
Patient aged >55 who have
- treatment-resistant dyspepsia
- Upper abdo pain with low Hb
- Raised platelets with nausea, vomiting, weight loss, reflux, dyspepsia, upper abdo pain
- Nausea, vomiting with weight loss, reflux, dyspepsia, upper abdo pain

351
Q

Management of patients who do not meed referral criteria?

A

Review meds
lifestyle advice
Trial of Full dose PPI for one month or test and treat approach

  • Test for H.pylori - using carbon-13 urea breath or stool antigen test.
  • Test of cure - no need to check for H.pylori eradication if symptoms have resolved.
352
Q

What visual field defect does a pituitary tumour cause?

A

Bitemporal hemianopia - upper quadrant defect

353
Q

What visual field defect does primary open angle glaucoma cause?

A

Unilateral peripheral visual field loss

354
Q

What visual field defect does a right stroke with right-sided hemiplegia cause?

A

Right homonymous hemianopia

355
Q

Left homonymous hemianopia means visual defect where?

A

Left ie lesion of the right optic tract.

356
Q

How do you remember homonymous quadrantanopias?

A

PITS

  • Parietal –> inferior
  • Temporal –> Superior
357
Q

What is an incongruous defect? Visual fields

A

Optic tract lesion

358
Q

What is a congruous defect - Visual fields?

A

Optic radiation lesion or occipital cortex

359
Q

What does a congruous defect mean?

A

Complete of symmetrical visual field loss

360
Q

What is an incongruous defect?

A

Incomplete of asymmetric defect.

361
Q

What is the first line medication treatment for parkinson’s if motor symptoms are affecting the patients QOL?

A

Levodopa

362
Q

What is the first line medication treatment for parkinson’s if motor symptoms are not affecting the patient’’s quality of life?

A

Dopamine agonists
Levodopa
Monoamine Oxidase B (MAO-B)

363
Q

Which parkinson medication has the most improvement for motor symptoms are activities of daily living?

A

Levodopa (also has mot motor complications)

364
Q

Which medication has the most adverse events (excessive sleepiness, hallucinations, impulse control disorders?)

A

Dopamine Agonists

365
Q

What is the next step in management if a patient develops symptoms whilst on optimal levodopa?

A

Add Dopamine agonist
MAO-B Inhibitor
COMT Inhibitor

366
Q

Which parkinson medications has the highest risk of hallucinations?

A

Dopamine agonists

367
Q

What are the risks associated with medications is not taken/absorbed (gastroenteritis)

A

Acute akinesia

Neuroleptic malignant syndrome

368
Q

If parkinson medications causes excessive sleepiness what must be considered?

A

Not driving

Modafinil if other strategies fail

369
Q

What should be done to manage orthostatic hypotension on parkinson’s medication?

A

Midodrine (peripheral alpha-adrenergic receptors to increase arterial resistance) can be considered

370
Q

How can you manage drooling of saliva in PD?

A

Glycopyrronium bromide

371
Q

What is Levodopa almost always combined with?

A 
Decarboxylase inhibitor (carbidopa/benserazide) 
(prevents metabolism peripehrally of levodopa to outside the brain and can reduce side effects)
372
Q

What are the common adverse effects of levodopa?

A 
Dry mouth
Anorexia
Palpitations 
Postural hypotension
Psychosis
373
Q

What are the adverse effects due to difficulty in achieving steady dose of levodopa?

A

End-of-dose wearing off - worsening symptoms at the end of dosage interval (delicine in motor activity)

374
Q

on-off phenomenon in PD?

A

variaction in motor performance (normal in on period and weakness and restricted mobility during off period)

375
Q

At peak dose of PD Medication what are patients at risk of?

A

Dystonia
Chorea
Athetosis (involuntary writhing movements)

376
Q

what is it important not to do when a patient is admitted to hospital with PD?

A

Do not stop levodopa

Switch to a dopamine agonist patch as rescue medications to prevent acute dystonia

377
Q

Give examples of dopamine receptor agonists?

A

Bromocriptine
Ropinirole
Cabergoline
Apomorphine

378
Q

Give examples of ergot-derived dopamine receptor agonists

A

Bromocriptine

Cabergoline

379
Q

What have Ergot derived dopamine receptors been associated with?

A

Pulomonary

Retroperitoneal and cardiac fibrosis

380
Q

What is required before starting patients on ergot-derivated D receptor agonists?

A

Echo
ESR
Creatinine
Chest XR

381
Q

What should patient’s be warned about the potential for dopamine receptor agnosits?

A

Impulse control disorder

Excessive daytime somnolence

382
Q

What is it more likely to cause than levodopa in older people ?

A

Hallucinations

Can also cause nasal congenstion/postural hypotension

383
Q

What is the MOA of MAO-B

A

Example - Selegiline

Inhibits breakdown of dopamine secreted by dopaminergic neurons

384
Q

What is the likely MOA of amantadine?

A

Not fully understood

Likely increases dopamine release and inhibitors uptake at dopaminergic synapses

385
Q

What are the side effects of amantadine?

A 
Ataxia
Slurred speech 
Confusion 
Dizziness 
Livedo Reticularis
386
Q

What are COMT Inh examples?

A

Entacapone

Tolcapone

387
Q

What is the MOA of COMT inhibitors?

A

COMT is an enzyme that breaks down dopamine and therefore may be used as an adjunct to levodopa therapy

388
Q

What is the MAO of antimuscarinics?

A 
block cholinergic receptors 
Now used to treatred drug induced parkinson's 
Helps tremor and rigidity 
Procyclidine 
Benxotropine 
Trihexyphenidyl
389
Q

patient presents with hypertension, hypokalaemia and alkalosis?

A

Primary Hyperaldosteronism

390
Q

What are the most common causes of Conns/Primary Hyperaldosteronism?

A

Adrenal Adenoma
Bilateral idiopathic adrenal hyperplasia
Adrenal Carcinoma

391
Q

What are the first investigations of primary hyperaldosteronism?

A

Aldosterone/Renin ratio
- Show high levels of aldosterone with low renin levels (negative feedback due to sodium retention from aldosterone)

Then HRCT Abdo and adrenal vein sampling to differentiate between unilateral and bilateral sources of aldosterone excess

392
Q

Regarding primary hyperaldosteronism how would you differentiate between unilateral adenoma and bilateral hyperplasia?

A

Adrenal Venous Sampling

393
Q

What is the management of primary hyperaldosteronism?

A

Adrenal adenoma: Surgery

Bilateral adrenocortical hyperplasia: Aldosterone antagonists e.g spironolactone

394
Q

Which medication can cause megaloblastic anaemia by altering folate metabolism?

A

Phenytoin

395
Q

What are the acute adverse effects of phenytoin?

A

Dizziness, diplopia, nystagmus, slurred speech

Then: confusion, seizures

396
Q

What are the chronic side effects of phenytoin?

A

Gingival hyperplasia (secondary to increase expression of platelet derived growth factor, PDGF)

Hirsutism
Coarsening of facial features
Drowsiness

397
Q

Other chronic side effects of phenytoin?

A 
Peripheral neuropathy 
Vit D metabolsim causes osteomalacia
Lymphadenopathy 
Dyskinesia 
Megaloblastic anaemia
Fever
Rashes 
Hepatitis 
Dupuytren's contracture 
Aplastic anaemia 
Drug-induced lupus
398
Q

How does phenytoin need to be monitored?

A

Not routinely
But trough levels immediately before dose if adjustment in phenytoin dose, suspected toxicity, detection of non-adherence to prescribed medications

399
Q

Slow growing patch of dry skin thickening to become plaque - biopsy shows lymphocytic and atypical t-cell infiltrates in the dermis, epidermis with some pautrier microabscesses

A

Mycosis Fungoides

400
Q

What is mycosis fungoides?

A

Rare, serious cutaneous form of T-cell lymphoma looking like eczema or psoriasis

Itchy,red patches, lesion tend to be of different colours in contrast to eczema/psoriasis where there is greater homogenicity.

401
Q

What is Harlequin ichthyosis?

A

Genetic condition present at birth

402
Q

What are symptoms associated with voiding urine in men?

A 
Hesistancy 
Poor or intermittent stream 
Straining 
Incomplete emptying 
terminal dribbling
403
Q

What are the symptoms associated with storage of urine in men?

A

Urgency
Frequency
Nocturia
Urinary incontinence

404
Q

What are the symptoms associated with post-micturiation?

A

Post-micturation dribbling

Sensation of incomplete emptying

405
Q

What examinations can be used to assess LUTS?

A

Urinalysis
DRE
PSA if needed

406
Q

Which guides are available for LUTS?

A

Urinary frequency-volume chart

IPSS

407
Q

What is the managemnt for voiding symptoms?

A

conservative: Pelvic floor muscle training
BLadder training
Fluid intake management

MEdical: Alpha-blocker: Tamsulosin, Alfuzosin, Doxazosin

408
Q

If enlarged prostate and moderate or severe symptoms how to manage?

A

Both alpha blocker

5-alpha reductase inhibitor (finasteride)

409
Q

What to do if there are mixed symptoms of voiding and storage not responding to an alpha blocker?

A

Antimuscarinic drug can be used - oxybutynin, tolterodine

410
Q

What is the manageement of overactive bladder?

A

Conservative management re: Fluid intake
BLadder retraining should be offered
Antimuscarinic drugs should be offered (Oxybutynin), tolterodine (immediate release), darifenacin
Mirabegron can be considered if first line failer

411
Q

Management for nocturia in men?

A

Moderating fluid intake
Furosemide 40mg late afternoon
Desmopressin

MSRA (1 decks)

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