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Year 6 > Passmedicine > Flashcards

Passmedicine Flashcards

1
Q

What are the cut off changes to know if you need to switch anti-HTNs with regards to creatinine and potassium when starting an ACE-inhibitor?

A

You are allowed a rise in creatinine up to 30%

Potassium is allowed to rise to 5.5 mmol/L

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2
Q

Generally speaking, most patients with chronic renal failure will have bilaterally small kidneys, however which 4 causes of CRF are the exception to this rule?

A
  1. Diabetic nephropathy
  2. PKD
  3. HIV-associated nephropathy
  4. Amyloidosis
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3
Q

What is the FEV1/FVC of healthy lungs?

A

70-80%

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4
Q

If the FEV1/FVC is <70% what does this imply?

A

Obstructive rather than restrictive cause

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5
Q

List some obstructive causes of lung disease (3)

A

COPD (Emphysema and Chronic bronchitis)
Asthma
Bronchiectasis

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6
Q

List some restrictive causes of lung disease (4)

A

Pulmonary fibrosis
Sarcoidosis
Pneumonia
Pulmonary oedema

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7
Q

What is total gas transfer (TLCO)?

A

Overall measure of gas transfer for the lungs from the alveoli into the capillaries

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8
Q

When would you expect to find a raised TLCO and why? (6)

A
  1. Asthma
  2. Left-to-right cardiac shunt
  3. Pulmonary haemorrhage (Wegener’s, Good pastures)
  4. Polycythaemia
  5. Hyperkinetic states
  6. Male gender, exercise
    This is because in these two - the problem is not in the alveoli/gas exchange, so the lungs compensate by improving gas exchange hence increasing TLCO
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9
Q

Give examples of conditions which cause a low TLCO (7)

A
  1. Pulmonary fibrosis
  2. Pulmonary oedema
  3. Emphysema
  4. Pneumonia
  5. Pulmonary embolus
  6. Anaemia
  7. Low cardiac output
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10
Q

In which patient is adenosine contraindicated for?

A

Asthma

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11
Q

Why is adenosine contraindicated in asthma?

A

Due to the risk of bronchospasm

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12
Q

What is the criteria for typical vs atypical angina?

A

Typical: all three of the symptoms:

  1. constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms
  2. precipitated by exertion
  3. relieved by rest or GTN in about 5 mins

Atypical - 2 out of the 3

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13
Q

List the 1st, 2nd and 3rd line investigations for pts in whom stable angina cannot be excluded by clinical assessment alone

A

1st line: CT coronary angio
2nd line: Non-invasive functional imaging (e.g. stress echo, CMR)
3rd line: invasive coronary angiography

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14
Q

In all 3 types of renal tubular acidosis, what would the blood gas show?

A

Hyperchloraemic metabolic acidosis with normal anion gap

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15
Q

What is the pathology in Renal tubular acidosis type 1?

A

The kidney’s are unable to secrete H+ into the distal tubule - therefore unable to excrete hydrogen ions

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16
Q

Which renal tubular acidosis types cause hypokalaemia.?

A

RTA type 1 and RTA type 2 - there is a loss of K+ ions

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17
Q

What are the complications of RTA type 1?

A

nephrocalcinosis and renal stones

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18
Q

What are the causes of RTA type 1? (4)

A
  1. Idiopathic
  2. Rheumatoid arthritis
  3. SLE
  4. Sjogren’s
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19
Q

Which part of the nephron is affected in RTA type 1?

A

Distal convoluted tubule

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20
Q

Which part of the nephron is affected in RTA type 2?

A

Proximal convoluted tubule

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21
Q

What is the pathology in RTA type 2?

A

decreased bicarbonate reabsorption in proximal tubule

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22
Q

What are the complications of RTA type 2?

A

Osteomalacia

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23
Q

What are the causes of RTA type 2?

A
  1. Idiopathic
  2. Fanconi’s syndrome
  3. Wilson’s disease
  4. Cystinosis
  5. Carbonic anhydrase inhibitors (topiramate)
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24
Q

In which type of renal tubular acidosis is potassium high?

A

RTA type 4

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25
Q

What is the pathology in RTA type 4?

A

reduction in aldosterone leads to reduction in proximal tubular ammonium excretion

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26
Q

What are the causes of RTA type 4?

A

Hypoaldosteronism (e.g. Addisons), Diabetes

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27
Q

What vaccinations do COPD patient require?

A

Annual flu vaccine

One-off Pneumococcal vaccine

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28
Q

If a patient presents with dyspepsia - What features/symptoms would warrant urgent referral for upper gastrointestinal endoscopy? (7)

A
  1. Anorexia
  2. Weight loss
  3. Anaemia
  4. Dysphagia
  5. Melaena
  6. Haematemesis
  7. Recent progression of symptoms
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29
Q

What are the different liver patient categories e.g. chronic liver disease …. (5)

A
  1. Chronic liver disease
  2. Liver cell failure
  3. Portal hypertension
  4. Encephalopathy
  5. Cholestasis
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30
Q

What are the signs of chronic stable liver disease? 6

A
  1. Spider naevi >5
  2. clubbing
  3. Palmer erythema
  4. Dupytren’s contracture
  5. Gynaecomastia
  6. Testicular atrophy
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31
Q

Where are spider naevi present?

A

In the chest, not the abdomen (SVC distribution)

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32
Q

What happens when you press down on a spider naevi?

A

the whole thing goes pale and then flushes from the inside and goes red again

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33
Q

What are the signs of portal hypertension? 4

A
  1. Splenomegaly
  2. Ascites
  3. Dilated veins on the abdomen (caput medusae)
  4. Haemtemesis/melaena
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34
Q

What are the signs of liver cell failure? 5

A
  1. Jaundice
  2. Leuconychia (low protein)
  3. Bruising (clotting/fibrinogen)
  4. Ascites
  5. Encephalopathy (flapping tremor caused by nitrogen)
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35
Q

What happens when you squeeze the blood out of the caput medusae vein by pushing on it?

A

The Blood fills the vein again from the umbilicus outwards

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36
Q

What is the other cause of distended abdominal veins on the abdomen?

A

Inferior vena cava obstruction

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37
Q

How can you differentiate between IVC obstruction and caput mudusae from portal hypertension?

A

Look at the vein below the umbillicus and press down on it - the blood should re-fill towards the umbillicus wherease in caput medusae the blood would refill away from the umbilicus

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38
Q

What are 5 causes of ascites?

A
  1. Portal hypertension /
  2. portal thrombosis
  3. IVC obstruction
  4. Budd chiari syndrome (hepatic vein obstruction)
  5. Ovarian malignancy
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39
Q

What are the features of Cholestasis?

A
  1. Excoriations (scratch marks)
  2. Pale stools
  3. Dark urine (negative for urobilinogen)
  4. Jaundice
  5. Xanthelasmata
  6. If they have PBC then anti-mitochrondrial antibodies may be positive
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40
Q

On palpation how can you differentiate between a spleen and the left kidney? (5)

A
  1. Spleen has a notch
  2. You cannot get above the spleen, but you can for the kidney
  3. Spleen = dull to percussion (but kidney is resonant due to overlying bowel
  4. Kidney is ballotable
  5. Spleen moves to RIF
    Kidney mores down when the pt inhales
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41
Q

When you ballot the kidney which hand should remain still?

A

The top hand

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42
Q

What are the causes of erythema nodosum?

A
  1. Sarcoidosis
  2. Strep infection
  3. IBD
  4. TB
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43
Q

Erythema multiforme (looks like targets)- which age groups tend to get them?

A

Children and young adults

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44
Q

What is the most common cause of erythema multiforme?

A

7-14 days after Herpes simplex

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45
Q

What are the other causes of erythema multiforme?

A

Mycoplasma
Strep
TB
Sulphonylurea

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46
Q

What is another name for really severe erythema multiforme?

A

Stevens- Johnson-Syndrome (this is erythema multiforme with mucosal ulceration and you get liver failure

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47
Q

What is erythema ab igne and what is it caused by?

A

It is brown patchy discolouration caused by chronic heat e.g. from repeated use of a hot water bottle
(No treatment is needed)

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48
Q

What is erythema margniatum associated with?

A

Acute rheumatic fever

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49
Q

What is erythema chronicium migrans associated with?

A

Lyme disease

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50
Q

What are the stages of diabetic retinopathy?

A
  1. Background
  2. Pre-proliferative
  3. Proliferative
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51
Q

What are the features of background diabetic retinopathy?

A
  1. Venodilation
  2. Microaneurysms
  3. Hard exudates (protein and lipid deposits)
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52
Q

What are the features of pre-proliferative diabetic retinopathy?

A
  1. Cotton wool spots (soft exudate) - these are ischaemic events
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53
Q

What are the features of proliferative diabetic retinopathy?

A

New vessel growth

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54
Q

If cotton wool spots are present what treatment is needed?

A

Laser

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55
Q

What are the 4 grades of hypertensive retinopathy?

A

Grade 1. Silver wiring and arteriolar narrowing
Grade 2. AV nipping
Grade 3. Flame shaped haemorrhages and cotton wool spots
Grade 4. Papilloedema

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56
Q

What is AV nipping?

A

When the artery crosses the vein, the vein gets narrower

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57
Q

If someone has a positive Romberg’s sign what does this tell you and what would you then want to check?
Romberg’s sign (stand with feet together and eyes closed - if they fall then it is positive)

A

It tells you they are very visually dependent when they walk and so you would want to check proprioception

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58
Q

What nerves are being tested when you ask someone to stand on their heels?

A

L4 and L5

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59
Q

What nerves are tested when you ask someone to stand on their toes?

A

S1 and S2

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60
Q

What is the gait like in an UMN lesion?

A

They will drag their feet and circumduct their legs (bilaterally)

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61
Q

What condition will cause positive Trendenlenburg sign?
Trendenlenburg sign - when you try and pick up you leg off the ground, the hip for that leg sinks so when these patients walk they waddling leaning their whole body weight from side to side)

A

myopathy - weakness in the gluteal muscles

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62
Q

What is the difference between cerebellar ataxic gait vs sensory ataxic gait?

A

Both are broad based

the difference is that in sensory they will stamp as they are not aware of where the floor is/how hard they are stepping

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63
Q

If there is a sensory ataxic gait and they are stamping, what sign might you want to check for?

A

Romberg’s

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64
Q

If it was a motor and sensory peripheral neuropathy then what might you notice on the gait?

A

Foot drop + broad-based gait w/ stamping

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65
Q

At the start of the neuro exam - what is it really important to ask the patient and why?

A

If they have any pain or numbness or tingling
(when you get to the examination you need to work from the numb area towards the normal area)
if they have a lot of pain, then you work from the normal area towards the area with pain because you dont want to plunge straight into the painful bit

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66
Q

What may Charcot’s joints be a sign of on inspection?

A

Peripheral neuropathy - if the sensation in the feet is down and they repeatedly crash their feet they can get Charcot’s joint

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67
Q

Is Spasticity UMN or LMN?

A

UMN

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68
Q

What is the descriptive term for spasticity?

A

Clasp knife

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69
Q

What are the features of spasticity?

A

Velocity dependent
Directional (given away by posture) - e.g. pushing the fingers is in is fine but then you try and open the fingers out it is much more difficult

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70
Q

What are the two types of rigidity in Parkinsons?

A

Lead pipe rigidity

Cog wheel rigidity

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71
Q

What is lead pipe rigidity?

A

When rigidity is smooth and consistent throughout

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72
Q

What is cog wheel rigidity?

A

If the rigidity is jerky then it is cog wheel which is thought to be rigidity superimposed onto an underlying tremor

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73
Q

Which nerve root does the triceps reflex test?

A

C7

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74
Q

Which nerve root does the biceps reflex test?

A

C5

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75
Q

Which nerve root does the brachioradialis reflex test?

A

C6

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76
Q

Which nerve root does the knee/patellar reflex test?

A

L3 and L4

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77
Q

Which nerve root does the ankle/achilles reflex test?

A

S1 and S2

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78
Q

When is a reflex considered absent?

A

when it is absent with reinforcement

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79
Q

If the lesion is below L1 why will it always be lower motor neurone?

A

Because the spinal cord stops at T12/L1

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80
Q

What are the causes of predominantly hypertriglyceridaemia?

A 
Alcohol
Diabetes type 1 and 2
Obesity
Drugs: Thiazide diuretics, non-selective beta blockers, unopposed oestrogen  
Liver disease
Chronic renal failure
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81
Q

What are the causes of predominantly hypercholesterolaemia?

A

Nephrotic syndrome
Cholestasis
Hypothyroidism

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82
Q

What is the sensory role of the median nerve?

A

Thumb
Index finger
Middle finger

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83
Q

What is the motor role of the median nerve?

A 
LOAF muscles
Lateral lumbricals, 
Opponens pollicis, 
Abductor pollicis brevis
Flexor policis brevis
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84
Q

What is Leishmania spread by?

A

Sandfly

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85
Q

Name the 3 different types of Leishmania

A

Cutaneous
Mucocutaneous
Visceral

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86
Q

What are the buzz words for Strep pneumonia cause of pneumonia?

A

Lobar

rusty coloured sputum

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87
Q

What are the buzz words for Haemophiulus influenzae cause of pneumonia?

A

COPD

Bronchiectasis

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88
Q

What are the buzz words for Klebsiella cause of pneumonia?

A

Alcoholic

red-currant jelly sputum

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89
Q

What are the buzz words for Staph aureus cause of pneumonia?

A

Post- influenza infection

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90
Q

What are the buzz words for Mycoplasma pneumoniae cause of pneumonia?

A

Atypical
Dry
Autoimmune haemolytic anaemia
Hyponatraemia

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91
Q

What are the buzz words for Pneumocystis jiroveci (PCP) cause of pneumonia?

A

Exertional desaturation
HIV
dry cough

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92
Q

What are the buzz words for Legionella pneumophilia cause of pneumonia?

A

Atypical
Air conditioning
Hyponatraemia
lymphopaenia

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93
Q

What type of organism is Pneumocytis jirovecii?

A

Fungus

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94
Q

Which of organisms cause cavitating in pnuemonia?(2)

A

Klebsiella

Staph aureus

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95
Q

What is the gold standard investigation for Bronchiectasis?

A

High resolution CT (signet ring- the airway is larger than the artery next to it)

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96
Q

How long do patients with bronchiectasis and infective exacerbation need antibiotics for compared to pneumonia?

A

Bronchiectasis - 14 day course of Abx

Pneumonia - 5 days if mild, 7-10 days if more severe

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97
Q

What are the features of a moderate asthma attack? (4)

A
  1. PEFR 50-75% best or predicted
  2. Speech normal
  3. RR < 25 / min
  4. Pulse < 110 bpm
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98
Q

What are the features of a severe asthma attack? (4)

A
  1. PEFR 33-50% best or predicted
  2. Can’t speak in full sentences
  3. RR > 25/ min
  4. Pulse >110 bpm
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99
Q

What are the features of life-threatening asthma attack? (5)

A
  1. PEFR < 33% best or predicted
  2. Oxygen sats < 92%
  3. Silent chest, cyanosis or feeble respiratory effort
  4. Bradycardia, dysrhythmia or hypotension
  5. Exhaustion, confusion or coma
    NOte: normal CO2 indicates life threatening also
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100
Q

CXR is not routinely done in an asthma attack, but when would you get one?

A
  1. Life threatening
  2. Not responding to treatment
  3. Suspected pneumothorax
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101
Q

In acute asthma attack, what is the criteria for admission to hospital?

A
  1. Life threatening
  2. Severe that is not responding to initial treatment
  3. Pregnancy
  4. Previous near fatal asthma attack
  5. Asthma attack despite being on oral corticosteroids
  6. Presentation at night time
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102
Q

Describe the criteria of how to administer SABA e.g. salbutamol or terbutaline in asthma attack

A

Modterate - give SABA via pressurised Metered dose inhaler

Severe - give nebulised SABA

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103
Q

Which patients in asthma attack should be given corticosteroid and what prescription?

A 
All patients 
Prednisolone
40-50mg 
Oral 
for 5 days (or until they recover)
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104
Q

Whilst the patient is on oral corticosteroid for asthma attack what is the advice regarding their normal asthma managment?

A

Continue as normal

even the inhaled corticosteroid can be taken whilst they are on oral prednisolone

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105
Q

Which patients in asthma attack receive ipratropium bromide?

A
  1. Severe or Life-threatening asthma

2. Non-responders to SABA and corticosteroids

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106
Q

Which asthma attack patients may receive mag sulf?

A

Severe or life threatening attacks

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107
Q

When might you consider aminophylline in asthma attack?

A

after consultation with a senior staff member

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108
Q

If asthma attack patients fail to respond, what could they receive in ITU?

A

Intubation and ventilation

ECMO - extracorporeal membrane oxygenation

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109
Q

What is the criteria for discharging a patient following an asthma attack? (3)

A
  1. They have been stable on their discharge medication (i.e. no nebulisers or oxygen) for 12–24 hours
  2. Inhaler technique checked and recorded
  3. PEF >75% of best or predicted
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110
Q

Which antibiotics can be used first line in COPD acute exacerbations?

A

Amoxicillin
Clarithromycin
Doxycycline

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111
Q

What is the corticosteroid prescription given in acute COPD exacerbation?

A

Prednisolone
30mg
Oral
for 5 days

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112
Q

How do you differentiate between acute bronchitis and pneumonia?

A

History
Sputum, wheeze, breathlessness may be absent in acute bronchitis whereas at least one tends to be present in pneumonia

Examination: No other focal chest signs (dullness to percussion, crepitations, bronchial breathing) in acute bronchitis other than wheeze.

Systemic features (malaise, myalgia, and fever) may be absent in acute bronchitis, whereas they tend to be present in pneumonia.

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113
Q

What are the contraindications to lung cancer surgery?

A

SVC obstruction, FEV < 1.5, MALIGNANT pleural effusion, and vocal cord paralysis

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114
Q

How is asthma diagnosed in patients >17 yo?

A
  1. Find out if the symptoms are better away from work/home - if yes then refer to specialist
  2. Spirometry with bronchodilator reversibility (BDR) testing - ALL PATIENTS
  3. FeNO (fractional exhaled nitric oxide) - ALL PATIENTS
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115
Q

How is asthma diagnosed in patients aged 5-16 yo?

A
  1. Spirometry with bronchodilator reversibility testing - ALL PATIENTS
  2. FeNO testing - ONLY if spirometry showed normal/obstructive picture with negative Bronchodilator reversibility (BDR) test
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116
Q

How is asthma diagnosed in patients <5 yo?

A

Based on clinical judgment - usually it would be viral induced wheeze at that age

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117
Q

What is considered positive FeNO?

A

adults > or = to 40 ppb

children > or = 35 ppb

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118
Q

What is considered positive BDR test?

A

adults:
1. improvement of FEV1 by 12% or more and
2. an increase in volume of 200ml or more
children:
1. improvement of FEV1 by 12% or more

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119
Q

What are the doses of low, moderate and high dose ICS in adults?

A

< or = 400 micrograms (mcg) = low dose
400 - 800 micrograms (mcg) = moderate
>800 micrograms (mcg) = high

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120
Q

How often should you consider stepping down asthma treatment?

A

Every 2-3 months

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121
Q

IF you decide to reduce the dose of ICS, by how much is advised in each step down?

A

25-50% at a time

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122
Q

When diagnosing COPD, when should spirometry be carried out?

A

Post-bronchodilator - FEV1/FVC ratio needs to be <70% even after the bronchodilator

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123
Q

In COPD diagnosis, what is the role of FBC?

A

To exclude secondary polycythaemia

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124
Q

What are the stages of COPD severity?

A 
FEV1 (of predicted): 
Mild >80 % (need symptoms to diagnose) 
Moderate 50-79%
Severe 30 -49% 
Very severe <30%
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125
Q

If a patient is on LTOT for COPD how long much supplementary oxygen should they be breathing per day?

A

15 hours

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126
Q

Which COPD patients should be assessed for LTOT?

A
  1. Very severe COPD (consider assessment if Severe)
  2. Cyanosis
  3. Polycythaemia
  4. Raised JVP
  5. Peripheral oedema
  6. Oxygen sats < or = 92% on air
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127
Q

What does the assessment for LTOT in COPD patients consist of?

A

ABG on 2 occasions at least 3 weeks apart

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128
Q

In which COPD patients do you then offer LTOT to?

A
  1. If O2 is <7.3kPa
  2. Is O2 is between 7.3 -8 kPa and they have one of the following
    - peripheral oedema
    - pulmonary HTN
    - secondary polycythaemia
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129
Q

Who should LTOT not be offered to?

A

Those who continue to smoke despite the smoking cessation support

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130
Q

What vaccinations do COPD patients need?

A
  1. annual influenza

2. one-off pneumococcal

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131
Q

Outline the 2-level Wells score of Pulmonary embolism

A
  1. Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins) = 3 points
  2. Alternative diagnosis less likely than PE = 3 points
  3. Tachycardia > 100bpm = 1.5 points
  4. Immobilisation for 3 days / surgery in the last 4 weeks = 1.5 points
  5. Previous DVT/PE = 1.5 points
  6. Haemoptysis = 1 point
  7. Malignancy (on Rx, Rx in the last 6 months, palliative) = 1 point
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132
Q

What is the interpretation of the 2 -level Wells score for PE?

A

< or = 4 points - PE unlikely

> 4 points - PE likely

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133
Q

If PE is likely according to Wells score, what do you do?

A

Arrange an immediate CTPA (if unable to occur soon then start anticoagulation)

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134
Q

If CTPA for PE is negative what do you do?

A

Proximal leg vein US if DVT is suspected

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135
Q

If PE is unlikely according to Wells score what do you do?

A

Arrange a D-dimer test (if it cannot be attained within 4 hours then start anticoagulation)

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136
Q

If the D- dimer for PE is positive, what do you do?

A

Arrange an immediate CTPA

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137
Q

If the D- dimer for PE is nagative, what do you do?

A

PE is unlikely, consider other diagnosis

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138
Q

If a patient has renal failure, which is used CTPA or V/Q scan in ?PE and why?

A

V/Q scan as you avoid the contrast which is used in CTPA

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139
Q

What are the ECG findings of PE?

A

S1Q3T3
S1 = Large S wave in lead 1
Q3 = Large Q wave in lead 3
T3 = T wave inversion in lead 3

RBBB
Right axis deviation
Sinus tachycardia

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140
Q

In ?PE, which patients should have a CXR?

A

All patients - important to exclude other pathology

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141
Q

What are the 8 criteria in the Pulmonary Embolism rule out criteria (PERC)?

A
  1. Age > or = 50
  2. Heart rate > or = to 100 bpm
  3. Oxygen < or = to 94%
  4. Previous PE or DVT
  5. Recent trauma or surgery in the last 4 weeks
  6. Haemoptysis
  7. Unilateral leg swelling
  8. Oestrogen use (COPC or contraceptives)
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142
Q

When should PERC be used?

A

When there is a low pre-test probability of PE but you want to be sure

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143
Q

How is PERC interpreted?

A

Negative means all 8 are negative - meaning less than 2% chance of PE
(if positive then do 2 level Wells score)

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144
Q

In PE how long should patients be anticoagulated for?

A

A minimum of 3 months

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145
Q

If a patient is unstable how do you investigate for PE?

A

CTPA

But if not able to get an urgent CTPA, you can get a bedside echo instead (RV dysfunction)

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146
Q

What is the management of PE in an unstable patient?

A

if PE found on CTPA/ RV dysfunction detected on echo
then pt needs URGENT REPERFUSION
1. UFH 10,000 Units IV - bolus
2. UFH continuous infusion
3. Consider if they need fluid resus (if SBP <90mmHg)
4. +/- vasoactive agents e.g. Noradrenaline if fluid resus is not successful
5. Consider if they need Oxygen
6. Whilst Heparin is still running, do pharmacological thrombolysis to break down the clot:
- Alteplase, Streptokinase, Urokinase (all IV)
7. Later on switch to anticoagulant (DOAC, LMWH, VKA)

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147
Q

What is the management of PE in a stable patient?

A

Confirmed or suspected PE - start DOAC (apixaban or rivaroxaban)

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148
Q

If a patient is unsuitable for Apixaban or Rivaroxaban, what are the alternatives?

A
  1. LMWH (5 days) + Dabigatran or Edoxaban, then after 5 day just the DOAC
  2. LMWH (5 days or until INR is > or = 2) + VKA then VKA alone
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149
Q

What 4 features might suggest COPD may be responsive to steroid (ICS)?

A
  1. Previous diagnosis of asthma or atopy
  2. Higher blood eosinophil count
  3. Substantial variation in FEV1 over time (>400ml)
  4. Substantial diurnal variation in PEFR (>20%)
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150
Q

When treating PE, you can risk stratify them using PESI (PE severity index) - which PESI classes are low vs intermediate?

A

PESI classes I and II = low

PESI classes III and IV = intermediate

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151
Q

If PESI is low risk - how do you manage them?

A

Rx at home- with oral anticoag
Safety net them about bleeding risk
Follow up in 1 week

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152
Q

Within the PESI intermediate group there are 2 groups intermediate-low and intermediate-high - how do you differentiate between the two groups?

A

Intermediate - low has either:
RV dysfunction on Echo
OR
Cardiac markers increased (e.g. BNP, trop)
Both simply indicate strain on the heart

Intermediate high has BOTH:
RV dysfunction on echo AND raised cardiac markers

153
Q

How do you manage intermediate patients?

A

Any intermediate patient will need to be admitted but if intermediate-high they will need close monitoring as they are at risk of being unstable

154
Q

How do you manage high risk?

A

Unstable management:
Unfractionate Heparin
+
Thrombolysis

155
Q

How do you define a provoke PE?

A

If the PE was preceded by a transient and major clinical RF in the last 3 months

156
Q

Which needs a longer course of anticoagulation provoked or unprovoked?

A

Unprovoked as they might have an underlying clotting disorder etc - we dont know why they had the PE

157
Q

In provoked PE, how long do you anticoagulate?

A

AT LEAST 3 months

except in cancer it is 3-6 months

158
Q

What is the cut off aspirate pH for knowing an NG tube is safe to use?

159
Q

If the aspirate pH is >5.5 on NG tube, what should you do?

A

CXR to confirm the position

160
Q

If the CO2 is normal on ABG of a COPD patient, what should the o2 sats targets be?

A

94-98% (instead of 88-92%)

161
Q

What are the two important investigations to get in pneumothorax?

A

CXR

Bloods - Clotting profile

162
Q

Why is clotting profile so important in Pneumothorax?

A

You need to know the bleeding risk before inserting a chest drain
Chest drain has a high bleeding risk and you can cause a haemothorax if clotting is derranged

163
Q

What are the 3 categories for causes of pneumothorax?

A
  1. Cystic causes e.g. Bullae in COPD, emphysema - if they rupture you get interruption of the pleural space
  2. Parenchymal necrosis - Massive PE, severe pneumonia/TB can also cause death of lung tissue and if this area is near the pleura you can interrupt the pleura and cause air to enter
  3. Iatrogenic/traumatic causes: Percutaneous biopsies, chest drains (e.g. for pleural effusion), Rib fractures
164
Q

How should the CXR for a ?pneumothorax be taken and why

A

In full expiration (not inspiration) - it allows the space between the two pleura to be as wide as possible

165
Q

In primary pneumothorax, which ones need percutaneous aspiration?

A

If they are symptomatic e.g. SOB
or
If the rim is >2cm

166
Q

Where is the insertion point for percutaneous aspiration in pneumothorax?

A

Mid-axillary line, 5th intercostal space

167
Q

How can you tell if percutaneous aspiration has been successful in pneumothorax?

A

Seeing the rim decrease on repeat CXR (<2cm) and the patient is no longer SOB
If this is the case you can discharge the patient after some observation

168
Q

What do you do if percutaneous aspiration has not been successful in pneumothorax?

A

Admit and do a chest drain

169
Q

What is another name for chest drain?

A

Thoracotomy tube

170
Q

What are the surgical options for a patient in which the chest drain has bene unsuccessful?

A
  1. Open thoracotomy

2. Video assisted thoracoscopic surgery (VATS)

171
Q

What is the management of primary pneumothorax with a rim <2cm and no SOB?

A

Discharge home after a period of observation

172
Q

What is the management of secondary pneumothorax with a rim <1cm (small)?

A

High flow oxygen

Admit and observe

173
Q

What is the management of secondary pneumothorax with a rim 1-2cm (moderate)?

A
  1. Percutaneous aspiration
    If successful then High flow oxygen, admit and observe
    If unsuccessful then Chest drain and admit
    If chest drain then unsuccessful –> surgical options
174
Q

What is the management of secondary pneumothorax with a rim >2cm (moderate) or SOB?

A

Proceed straight to chest drain - no percutaneous aspiration
If unsuccessful then surgical options

175
Q

Can you do percutaneous aspiration twice?

A

NO!! go straight for chest drain

176
Q

What is the difference between empyema and abscess?

A

Abscess is pus in a new cavity

Empyema literally means ‘bag of pus’ but it is specifically in an already existing cavity such as the pleural space

177
Q

What is the management of Tension Pneumothorax (non-traumatic)?

A
  1. Peri-arrest call
  2. Immediate decompression using large bore cannula + high flow o2
  3. Chest drain + admit
178
Q

Where do you insert the large bore cannula for immediate decompression in Tension Pneumothorax (non-traumatic)?

A

2nd ICS in MCL

179
Q

What should the advice be after a pneumothorax?

A

STOP SMOKING (it is a major RF)
No diving
No flying <1wk after CXR resolution

180
Q

What is the safety triangle for insertion of a chest drain?

A
  1. Axilla (superior boundary)
  2. Lateral edge of the pectoralis major (medial boundary)
  3. 5th intercostal space (inferior boundary) and
  4. anterior border or latissimus dorsi (lateral boundary)
    (even though “triangle” it has 4 sides)
181
Q

What diagnosis is important to consider following acute deterioration after ventilating a patient?

A

Tension pneumothorax

182
Q

Which pts should be referred for 2ww for lung cancer?

A
  1. CXR findings suggest lung cancer

2. >40yo with unexplained haemoptysis

183
Q

Which pts should be offered an urgent CXR (within 2wks) for ?lung cancer?

A

Age >40 (with 2 or more of the following if never smoked or 1 or more of the following if they have ever smoked):

  1. cough
  2. SOB
  3. chest pain
  4. fatigue
  5. weight loss
  6. appetite loss
184
Q

Which pts should you consider doing an urgent CXR for ?lung cancer?

A

Age >40 and any 1 of the following:

  1. persistent or recurrent chest infection
  2. finger clubbing
  3. supraclavicular lymphadenopathy or persistent cervical lymphadenopathy
  4. chest signs consistent with lung cancer
  5. thrombocytosis
185
Q

In pleural effusion - what protein level differentiates between transudate and exudate?

A

30g/L
i.e. >30g/L protein level = exudate
<30 g/L protein level = transudate

186
Q

Between what fluid protein level would you use Light’’s criteria in pleural effusion?

A

25 -35g/L (this is a grey zone where you cannot be certain so Lights criteria is useful

187
Q

What is Light’s criteria for pleural effusion?

A

If any of the following apply then it is exudate:
fluid protein : serum protein >0.5
fluid LDH : serum LDH > 0.6
fluid LDH > two-thirds the ULN of serum LDH

188
Q

What is the transfusion threshold for patients with ACS?

189
Q

What is the transfusion threshold in the general patient population?

190
Q

In pleural effusion what are the differentials for exudate?

A

Malignancy (lung cancer, mets, mesothelioma, lymphoma), infection (TB, pneumonia), inflammatory (SLE, Rheumatoid arthritis), Pulmonary infarct, pulmonary embolism

191
Q

In pleural effusion, what is the pathophysiology of exudate?

A

Increased microvascular permeability

192
Q

In pleural effusion what is the pathophysiology of transudate?

A

Increased hydrostatic pressure

Reduced osmotic pressure

193
Q

What are the differentials for transudate in pleural effusion?

A 
Heart failure 
Liver failure (cirrhosis) 
Nephrotic syndrome 
Meig's syndrome 
Trauma 
Hypoalbuminaemia
194
Q

What perianal features do you find in Crohn’s disease?

A

Skin tags

ulcers

195
Q

What the risk factors for Crohn’s?

A

FH

Smoking

196
Q

What are the extra GI manifestations for Crohn’s disease?

A

Skin - pyoderman gangrenosum, erythema nodosum
Eyes - uveitis, episcleritis
Joints - arthritis

197
Q

What is the most common extra GI manifestation of Crohn’s?

A

episcleritis

198
Q

What bloods do you want to do to investigate Crohn’s?

A 
FBC (anaemia) 
CRP (good marker of disease activity) 
Ferritin 
B12, Folate, Vitamin D (important as the malabsorption from the gut may lead to deficiency) 
LFTs (albumin)
199
Q

What stool investigations do you want to do for ?Crohn’s?

A

Stool MC&S - to exclude infection e.g. ?c.diff

Faecal calprotectin

200
Q

What is faecal calprotectin?

A

It is an inflammatory marker for inflammation in the gut - but is not specific
- it is a good rule out - because fi negative then it means NO Inflammation and IBD is unlikely

201
Q

If faecal caprotectin is raised in the work up to IBD, what IVx comes next?

A

Colonoscopy + histology

202
Q

Why is b12 always replaced before folate?

A

if folate is replaced first it can lead to subacute combined degeneration of the spinal cord

203
Q

When might you use imaging in diagnosis of Crohn’s and what imaging options are there?

A

If colonoscopy doesn’t detect anything

Barium enema of small bowel, MRI, capsule endoscopy

204
Q

What else can imagine be useful for in Crohn’s disease?

A

Complications

205
Q

List the imaging used in the complications of Crohn’s?

A 
Pelvic MRI (perianal disease) 
CT  Abdo + Pelvis (abscesses, fistulae, obstruction) 
AXR (dilation/obstruction)
206
Q

Describe the treatment ladder for inducing remission in Crohn’s disease

A
  1. Glucocorticoids (oral, topical, IV)
  2. 5-ASA (you stop the steroids)
  3. Add on: Azathioprine/ Mercaptopurine/ Methotrexate (this will be commonly used in those with recurrent flares (2 or more in 12 months)
  4. Biologic agents: Infliximab or Adalimumab
207
Q

When might you be inclined to use topical 5-ASA as 1st line for inducing remission in Crohn’s disease (rather than glucocorticoid)?

A

If the disease is limited to the perianal area

208
Q

What does 5-ASA stand fo and Name 2 examples of 5-ASAs

A

Aminosalicylates
Mesalazine
Olsalazine

209
Q

If you are going to give patients Azathioprine or Mercaptopurine, what is it important to measure before starting?

A

TPMT levels

210
Q

Describe the treatment ladder for maintaining remission in Crohn’s disease

A
  1. STOP SMOKING - really important
  2. Azathioprine or mercaptopurine
  3. Methotrexate
  4. 5-ASA (often given if the person has had operations for their Crohn’s disease)
211
Q

What % of people with Crohn’s disease require surgery?

212
Q

In Crohn’s what is the most common surgery performed and for what?

A

Ileocaecal resection for terminal ileum disease

213
Q

Which complications of Crohn’s might require surgery?

A
  1. Strictures - ballon dilatations
  2. Fistulae
  3. Perforation
214
Q

How much in advance before an upper GI endoscopy do PPIs need to be stopped?

A

2 weeks before

215
Q

What is the triad of symptoms in Budd Chiari syndrome?

A
  1. Sudden onset abdo pain
  2. Ascites
  3. Tender hepatomegaly (Can also get splenomegaly from the portal hypertension)
216
Q

Where do you usually get abdo pain in UC?

A

Left lower quadrant, but can be elsewhere

217
Q

Which extra-GI manifestation of IBD is more common in UC than Crohn’s?

A

uveitis (instead of episcleritis)

218
Q

What is the additional extra-GI manifestation that you see in UC but not in Crohn’s?

219
Q

In UC, you shouldn’t see disease beyond which point?

A

The ileum (not beyond the ileocaecal vavle)

220
Q

However, when might you see disease in UC beyond the ileum (from the ileocaecal valve)?

A

In backwash ileitis

221
Q

Which imaging can be used to really help you distinguish between UC and Crohn’s

A

Cross sectional imaging using CT/MRI/Small bowel US

222
Q

Management of UC is based on which 2 factors?

A

The extent of the disease

The severity of the disease

223
Q

What are the different options for extent of the disease in UC?

A

proctitis (just the rectum), protosigmoiditis (involves the sigmoid), left sided UC (has gone all the way up)

224
Q

What 3 things determine severity of UC?

A

Stool frequency
Blood in stool
Endoscopic appearance

225
Q

Classify UC into mild, moderate and severe based on stool frequency

A

Mild - 1-2/day (more than normal)
Moderate - 3-4/day (more than normal)
Severe - >5/day (more than normal)

226
Q

Classify UC into mild, moderate and severe based on blood in stool

A

Mild - Streaks of blood
Moderate - Obvious blood with stool most of the time
Severe - Blood without stool (just blood coming out)

227
Q

Classify UC into mild, moderate and severe based on endoscopic appearance

A

Mild - Erythema, mild friability
Moderate - Marked erythema, loss of vascular patterns, erosions
Severe - Spontaneous bleeding, ulceration

228
Q

Describe the mangement of mild-moderate ACTIVE UC disease

A
  1. Topical 5-ASA
  2. Add on oral 5-ASA (if incomplete response after 4 weeks)
  3. Switch or add topical steroids (if incomplete response)
  4. If that still doesn’t work then oral steroids (jump straight to step 4 if severe UC)
  5. Biological agents (infliximab) - only if incomplete response to oral steroids after 2 weeks
229
Q

What is maintenance therapy in UC involving proctosigmoiditis?

A

Topical 5-ASA +/- oral 5 ASA

230
Q

What is maintenance therapy for left sided UC?

A

oral ASA (As topical will not work for back enough)

231
Q

In the maintenance of UC, at what point do you consider azathioprine/mercaptopurine?

A

If more than 2 flares per year

232
Q

Describe the management of severe ACTIVE UC disease (this is not for an acute flare but someone who is systemically well but just has severe disease )

A
  1. Consider for admission
  2. Oral steroids
  3. Biological agents (infliximab) - only if incomplete response to oral steroids after 2 weeks
233
Q

In Crohn’s disease where do you tend to get the abdominal pain?

A

Right iliac fossa

remember: UC - left lower quadrant pain

234
Q

Compare the complications in UC vs Crohn’s

A

Crohn’s: fistulae, abscesses, gallstones

UC: there is a higher risk of Colorectal cancer, PSC

235
Q

Why is gallstones more of a problem in Crohn’s compared to UC?

A

The terminal ileum is involved with bile acid resorption, so if you have terminal ileum disease in Crohn’s then more prone to gallstones

236
Q

Compare the histology in UC vs Crohn’s

A

Crohn’s: inflammaiton all layers, increased goblet cells and granulomas
UC: inflammation limited to mucosa and submucosa, crypt abscesses

237
Q

Compare the endoscopy findings in UC vs Crohn’s

A

Crohn’s : Deep ulcers, skip lesions, cobblestone mucosa

UC: Superficial ulceration, pseudopolyps

238
Q

Compare the barium study findings in UC vs Crohn’s

A

Crohn’s: kantor’s sign (strictures), rose thorn mucosa (ulcers)
UC: loss of haustra, pseudopolyps, lead-pipe colon

239
Q

What does a serum albumin ascites gradient (SAAG) help you distinguish between?

A

A peritoneal (<11) vs non-peritonial (>11) cause of ascites

240
Q

List some non-peritoneal causes of ascites

A

Budd Chiari
Nephrotic syndrome
Liver cirrhosis

241
Q

List some peritoneal causes of ascites

A

TB Peritonitis

Peritoneal mesothelioma

242
Q

Which is medication is used for ascites secondary to liver cirrhosis?

A

Spironolactone

243
Q

Upon diagnosis of which two conditions should you also then screen for coeliac disease?

A

T1DM
autoimmune thyroid disease
(this is cause there is a link between these 2 and coeliac disease)

244
Q

Which vaccine does Coeliac UK recommend for those with coeliac? (And state the regimen)

A

Pneumococcal vaccine upon diagnosis and a booster every 5 years

245
Q

Why do coeliac patients receive a pneumococcal vaccine?

A

They are prone to overwhelming pneumococcal sepsis due to hyposplenism

246
Q

Which bloods should those with coeliac disease have annually?

A
  1. FBC
  2. Ferritin
  3. TFTs
  4. LFTs
  5. B12
  6. Folate
247
Q

What bloods should you take for someone with an acute flare of IBD?

A 
FBC 
CRP 
U and E 
LFTs 
Additonal bloods: 
Hep B, Hep C, HIV, VZV, TB screen
248
Q

What is the reason for doing additional bloods such as Hep B and C and HIV screen for a pt having an acute flare of IBD?

A

In case they need to be started on a biologic agent

249
Q

How do you initially manage an acute flare of IBD?

A

A-E approach

NBM + IV fluids + IV hydrocortisone (100mg) + LMWH

250
Q

If there is no improvement within 72 hours of initial management for acute flare of IBD, what is the next step?

A 
IV infliximab 
IV ciclosporin (UC)
251
Q

During the management an acute flare of IBD, it is important to always consider the need for what?

A

Emergency surgery

252
Q

What is the referral criteria for 2ww OGD ?

A

Any dysphagia
OR
>55 yo with ALARM symptoms

253
Q

What are the alarm symptoms?

A 
Anaemia 
Loss of weight
Anorexia 
Recent/progressive symptoms 
Malaena/Haemoatemsis 
Swallowing difficulty (dysphagia)
254
Q

If someone presents with dyspepsia, what is the lifestyle advice?

A

Weight loss
Smoking cessation
Reduce alcohol
Review medications - NSAIDs and steroids

255
Q

What is the medical management for dyspepsia?

A

Test for H. pyloria, whilst you are waiting start them on a 4 week trial of PPI

256
Q

If a patient with dyspepsia has trialled the 4 weeks of PPI and their H.pyloria testing returned as negative, what is the next step?

A

Try a different medication
H2-receptor antagonist e.g. ranitidine
If that also doesn’t work (i.e. optimal medical management has failed, then refer for endoscopy)

257
Q

If you use H. pylori eradication therapy, in which patients would you do an H.pylori retest?

A
  • Poor compliance
  • Still symptomatic
  • Hx of peptic ulcer disease
258
Q

How long do you give H. pylori eradication therapy for?

259
Q

What is the 2nd line H.pylori eradication therapy for someone who is not pen allergic?

A

PPI, metronidazole, clarithromycin

note first line would have been PPI, amoxicillin, clarithromycin

260
Q

What is 2nd line H. pylori eradication in someone who is pen allergic?

A

PPI, metronidazole, levofloxacin

261
Q

What are the risk factors for GORD?

A

Smoking
Obesity
Alcohol
Male

262
Q

If a patient has dyspepsia and is sent for ODG and it is found they have GORD (and hence oesophagitis on OGD) - what is the treatment?

A

Conservative : weight loss, stress reduction, alcohol reduction, sleep with head of bed raised
Medication: PPI for 8 weeks

263
Q

What are the risk for peptic ulcer disease?

A

H. pylori
NSAIDs
Stress (physiological e.g. shock, sepsis, burns)
Zollinger-Ellison syndrome

264
Q

How do you manage peptic ulcer disease?

A

Test for H.pylori, and if +ve then eradicatino therapy

If -ve, full dose PPI for 4-8 weeks

265
Q

HOw do you manage a peptic ulcer if it is associated with both NSAIDs and H.pylori?

A

2 months of full dose PPI before you then give eradiacation therapy

266
Q

What is the follow up for peptic ulcer disease?

A

Repeat H.pylori testing in 6-8 weeks

Repeat endoscopy in 6-8 weeks (only if it was gastric ulcer)

267
Q

GI bleeding is more common with which type of peptic ulcer and why?

A

dudodenal ulcers as they can erode the gastroduodenal artery

268
Q

What are the complications of peptic ulcer?

A

GI bleed
Perforation
Gastric outlet obstruction (if Stricture/ scarring/ pyloric stenosis/ duodenal stenosis from inflammation)

269
Q

What are the RF for barrets oesophagus?

A

GORD
Smoking
Male
Obesity

270
Q

What is the management of barrets oeseophagus?

A

Full dose PPI

Endoscopic surveillance

271
Q

How often is the endoscsopic surveillance in barrets oesophagus?

A

every 3-5 years

272
Q

If dysplasia is detected within barrets oesophagus, what is the management?

A

endoscopic mucosal resection or radiofrequency ablation

273
Q

How can you categorise Upper GI bleed?

A

Variceal vs non-variceal

274
Q

What are the variceal upper GI bleeds?

A

Oesophageal varices

Gastric varices

275
Q

Non-variceal bleeds (5)

A
  1. Mallory Weiss tear
  2. Boerhaave’s
  3. Peptic ulcer disease
  4. Malignancy
  5. Angiodysplasia
276
Q

What bloods do you want to take in an upper GI bleed?

A 
FBC (anaemia) 
U and E 
LFTs 
Clotting 
VBG/ABG 
G+S 
Cross match
277
Q

What is the risk assessment for upper GI bleed?

A

Glasgow Blatchford scale

278
Q

How do you manage a non-variceal bleed?

A

Resuscitate then OGD in 24 hours
(fi severe bleed then OGD immediately after resus)
Do NOT give PPIs before endoscopy as it can affect what you see

279
Q

If on OCG during Upper GI bleed, they detect a bleeding peptic ulcer what can they do?

A
  1. adrenaline injection to the ulcer
  2. sclerosant injections
  3. endoclips

these are all during the endoscopy

280
Q

If they have a bleeding peptic ulcer in Upper GI bleed what prescription of PPI would you give?

A

IV PPI for 72 hours

281
Q

What is the treatment for variceal bleed?

A

Resus
Prophylactic antibiotics
Terlipressin
Urgent OGD

282
Q

If varices are detected on OGD what can be done during the endoscopy?

A 
Band ligation 
(it is better for varices over sclerotherapy)
283
Q

What is the triad of acute liver failure?

A

Jaundice
Encephalopathy
Coagulopathy

284
Q

What are the causes of acute liver failure?

A

Infections - Hep A-B (esp A and B), EBV/CMV, leptospirosis
Toxins - Paracetamol, drug induced
Vascular - Budd chiari, veno-occlusive disease
Others - Wilson disease, autoimmune hepatitis, lymphoma

285
Q

Where are platelets made?

A

By the liver

286
Q

What imaging might you want to do if ?acute liver failrue?

A

Abdo USS - liver texture, vessel flow, splenic size

CTAP (CT abdo pelvis) - liver texture and volume, vessel patency

287
Q

What is the criteria for diagnosing acute kidney injury?

A
  1. increase in Creatinine 26nanomol/L in 48 hours
  2. increase in creatinine by more than 50% in 7 days
  3. urine output <0.5/kg/hour for more than 6 hours
288
Q

How does calcitonin reduce serum calcium levels?

A

It inhibits osteoclast activity

289
Q

Why are the bones at risk of osteomalacia if a patient has a high phopshate?

A

PTH is released to reduce the phosphate but in the process PTH also breaks down bone

290
Q

What ‘standard’ bloods do you want to request in acute liver failure and justify each

A

FBC - platelets (produced by liver- indicates function)
U and Es - hepatorenal syndrome (if severe)
LFTs - may help identify cause
ABG - pH and lactate (can indicate severity)
Clotting - synthetic function
Group and save - transfusions may be required

291
Q

Which additional bloods do you want to check for helping to identify the cause of actue liver failure?

A
  1. Paracetamol levels
  2. Viral hepatitis serology
  3. ANA/Anti-smooth muscle (autoimmune hepatitis)
  4. Urinary copper, serum ceruloplasmin (Wilson’s disease)
292
Q

What is the King’s College criteria can be used to determine need for liver transplant in acute liver failure due to PARACETAMOL OVERDOSE?

A

King’s College criteria
ph <7.3
OR
INR >6.5 + creatinine >300 + grade 4 encephalopathy

293
Q

What is the King’s College criteria can be used to determine need for liver transplant in acute liver failure NOT due to PARACETAMOL OVERDOSE?

A 
INR >6.5 
OR 
Any 3 of: 
- Age <10, Age >40 
- time from jaundice to encephalopathy >7 
- INR >3.5 
- Bilirubin >300 
- non A or B viral hepatitis 
- drug induced hepatitis
294
Q

Where should patients with acute liver failure be treated?

295
Q

What is the treatment for acute liver failure caused by autoimmune hepatitis?

A

methyprednisolone

296
Q

What is the treatment for acute liver failure caused by Budd Chiari syndrome?

A

Anticoagulation

297
Q

What is the surveillance for those with cirrhosis (and hence an increased risk of HCC)?

A

Anyone with confirmed cirrhosis should have 6 monthly USS and AFP to screen for HCC

298
Q

At diagnosis of cirrhosis why do patients need an OGD?

A

To check for oesophageal varices

299
Q

If there are no oesophageal varices upon OGD (after diagnosis of cirrhosis) what is the surveillance?

A

OGDs every 3 years

300
Q

If varices are detected on OGD (after cirrhosis diagnosis) but are not bleeding - what prophylaxis can you give?

A

Propranolol

301
Q

Aside from HCC and oesophageal varices what is the other big complication of cirrhosis?

302
Q

What is first line treatment to ascites?

A

Diuretic - spironolactone

303
Q

If ascites is refractory to diuretic treatment, what might you do next?

A

Therapeutic paracentesis (come in regularly to get ascitic drains)

304
Q

What is a TIPSS procedure?

A

Transjugular Intrahepatic Portosystemic shunt (helps to divert blood away from the portal vein so that you can reduce the portal HTN

305
Q

Give some examples of triggers for decompensated liver disease

A

Alcohol/drugs
Sepsis/Infection
GI bleed
Ischaemic injury

306
Q

If in ascitic tap, the neutrophils are >250 what does this mean?

A

Spontaneous Bacterial peritonitis

307
Q

What is the treatment for SBP?

A

IV antibiotics and Human Albumin Solution

308
Q

What is the treatment for hepatic encephalopathy?

A

Lactuloase and

Rifaximin

309
Q

What does lactulose do, to help treat hepatic encephalopathy?

A

It promotes excretion of ammonia

310
Q

What does Rifaximin do to help treat encephalopathy?

A

Decreases production of ammonia

311
Q

What are the 3 stages of alcoholic liver disease?

A

Steatosis (fatty liver)
Alcoholic hepatitis (inflammation and necrosis)
Cirrhrosis

312
Q

What is the management for alcoholic liver disease?

A

Alcohol abstinence +/- withdrawal management
Nutritional supplements: Thiamine/pabrinex
Steroids: for alcoholic hepatitis

313
Q

Which hepatitis is always acute?

314
Q

What is the incubation time of Hep A?

315
Q

Which hepatitis is dangerous in pregnant women?

316
Q

What is the treatment of Hep A and E?

A

supportive treatment, self- limiting

317
Q

What makes Hep B different to the other Hep viruses?

A

It is a DNA virus - the others are RNA

318
Q

Which part of Hep B serology is a marker of severity?

319
Q

How long does anti HBc IgM remain high for?

A

6 months (remember the IgM is seen in the acute infection whilst the IgG is seen in the chronic infection)

320
Q

What is the treatment for Hep B ?

A

Supportive - 90% of adults will clear it

321
Q

When can Hep D infect someone and why?

A

It can either co-infect someone with Hep B simultaneously or it can superinfect an individual that already has Hep B
This is because it is an incomplete RNA virus

322
Q

Which Hepatitis is curable?

A

Hep C - treated with antivirals based on the virus genotype

323
Q

What investigations would you do for Hep C?

A

Hep C PCR

Viral genotyping - dictates treatment

324
Q

What is the main complication with Hep C?

325
Q

Which HLA is autoimmune hep associated with?

A

HLA DR3

HLA B8

326
Q

What are the antibodies to look out for in autoimmune hepatitis?

A

ANA
anti- smooth muscle antibodies (SMA)
anti LKM antibodies

327
Q

What is the treatment of autoimmune hepatitis?

A
  1. Steroids
  2. immunosuppressants e.g. azathioprine
  3. live transplant if really bad
328
Q

What do you need in order to see Kaiser Fleischer rings

A

A slit lamp

329
Q

What will the copper IVx look like for Wilsons disease?

A

reduced serum caeruloplasmin
reduced serum copper
increased 24 hr urinary copper

330
Q

Penicillamine used in the Rx of Wilsons disease does what?

A

copper chelating agent

331
Q

Which antibodies for PBC?

A

AMA - main one
SMA
Raised IgM

332
Q

What is the treatment of PBC?

A

itching - cholestyramine
Ursodeoxycholic acid - for bile salts
transplant

333
Q

Which autoimmune condition is associated with cholangiocarcinoma

334
Q

Which ANCA does PSC have?

335
Q

What might liver biopsy show in PSC?

A

onion-skinning - concentric circles around bile duct of fibrosis

336
Q

Which UTIs are complicated?

A

Persistent infection
Rx failure
Recurrent infection
Atypical organism

337
Q

What are upper urinary tract infection?

A

Ureter or kidney (pyelonephritis)

338
Q

What is the time period to define catheter associate UTI?

A

symptoms within 48 hours

339
Q

What is the eGFR cut off for CKD? and what other features help to diagnose CKD?

A

PERSISTENT eGFR <60

  • urinary albumin:creatinine >3
  • urine sediment abnormalities
  • structural abnormalities
340
Q

What are the first things you want to assess in AKI?

A
  1. Assess the volume status - this will help indicate if they are pre-renal, renal or post-renal
  2. Review the DH and stop any nephrotoxic drugs
341
Q

What is the management for pre-renal AKI?

A

Fluid resus and treat the underlying cause

342
Q

What is the management for renal AKI?

A

Investigate the cause (e.g. ANA, ANCA)
Refer to specialist
Consider dialysis

343
Q

What is the management for post-renal AKI?

A

If they have a catheter, flush it and see if still draining - if not then put a new one
Catheterise the patient if they have post-renal without a catheter- this will relieve the urinary retention

344
Q

What is the criteria for receiving dialysis in AKI?

A

Refractory pulmonary oedema
persistent hyperkalaemia
Metabolic acidosis
Uraemic complications e.g. pericarditis

345
Q

What are the 3 main causes of CKD?

A

HTN
Diabetes
Glomerular disease

346
Q

What pneumonic can be used to remember the complications of CKD?

347
Q

What does CRF HEALS stand for?

A

Cardiovascular disease
Renal osteodystrophy
Fluid (oedema)

Hypertension
Electrolyte abnormalities 
Anaemia 
Leg restlessness 
Sensory neuropathy
348
Q

Which medications may be involved in the management of CKD?

A 
Statin 
Antiplatelet therapy 
Vitamin D and calcium suppplements 
Phosphate binders 
Diuretics 
EPO (if iron def)
349
Q

What are the blood pressure targets in CKD?

350
Q

What are the BP targets in T2DM?

351
Q

What are the BP targets in T1DM?

A

<135/85
But if T1DM and albuminuria then <130/80
But if T1DM and 2 or more features of metabolic syndrome then <130/80

352
Q

What foods should those with CKD avoid?

A

Those which are potassium and phosphate rich

353
Q

Which foods have high potassium?

A

Bananas, oranges, potatoes and sweet potatoes

354
Q

Which foods have high phosphate?

A

Chicken, turkey, seafood, dairy

355
Q

What are the primary causes of nephrotic syndrome?

A

Minimal change disease
Focal segmental glomerulonephritis
Membranous glomerulonephritis

356
Q

What are the secondary causes of nephrotic syndrome?

A

Diabetes
SLE
Amyloid
Hep B/C

357
Q

What are the primary causes of nephritis syndrome

A

Membranoproliferative glomerulonephritis

Rapidly proliferative glomerulonephritis (Crescentic)

358
Q

What are the secondary causes of nephritis syndrome?

A 
Post-streptococcal glomerulonephtritis 
IgA nephropathy
Vasculitis 
SLE 
Good pasture's syndrome
359
Q

What 3 things classify nephrotic syndrome

A

Proteinuria (>3g/24 hours)
Hypoalbuminaemia
Oedema
(Hyperlipidaemia)

360
Q

What 3 things classify nephritis syndrome?

A

Hypertention
Haematuria
Oliguria /Proteinuria

361
Q

What is the most severe glomerulonephritis with poor prognosis?

A

Rapidly progressive/proliferative

362
Q

What is the difference between haemodialysis and haemfiltration?

A

Dialysis is vis diffusion

Filtration is via convection

363
Q

What is the triple therapy for maintenance of Renal replacement?

A
  1. Calcineurin inhibitor e.g. Tacrolimus
  2. Anti-metabolite e.g. azathioprirne
  3. Prednisolone
    (all are immunosuppressants)
364
Q

What are the indications for renal replacement therapy in CKD?

A

eGFR <10

symptomatic complications from the kidney disease

365
Q

What is the acronym for causes of a normal anion gap? (expand it as well)

A 
ABCD
Addisons 
Bicarb loss 
Chloride 
Drugs
366
Q

What are the features of L3 nerve root compression?

A

Sensory loss over anterior thigh
Weak quadriceps
Reduced knee reflex
Positive femoral stretch test

367
Q

What are the features of L4 nerve root compression?

A

Sensory loss anterior aspect of knee
Weak quadriceps
Reduced knee reflex
Positive femoral stretch test

368
Q

What are the features of L5 nerve root compression?

A

Sensory loss dorsum of foot
Weakness in foot and big toe dorsiflexion
Reflexes intact
Positive sciatic nerve stretch test

369
Q

What are the features of S1 nerve root compression?

A

Sensory loss posterolateral aspect of leg and lateral aspect of foot
Weakness in plantar flexion of foot
Reduced ankle reflex
Positive sciatic nerve stretch test

370
Q

What are the clinical signs of a fracture?

A 
Pain
Swelling
Deformity
Crepitation
Adjacent structural damage: nerve, vessel, ligament, tendon
371
Q

What are the five steps in describing a fracture?

A
  1. Location i.e. which bone + which part of the bone
  2. Pieces: Simple/multifragmentary
  3. Pattern: Transverse/oblique/spiral
  4. Displaced/undisplaced
  5. Translated/Angulated
372
Q

State the name of translation away from the midline and state the term for angulation away from the midline (coronal plane)

A

Lateral translation

Valgus

373
Q

State the name of translation toward the midline and state the term for angulation toward the midline (coronal plane)

A

Medial translation

Varus

374
Q

How would you describe translation and angulation in the sagittal plane i.e. the sideways plane

A

Anterior or posterior translation

Dorsal or Volar angulation

375
Q

What are the criteria for starting Ivabradine?

A
  1. the patient is already on suitable therapy (ACE-inhibitor, beta-blocker + aldosterone antagonist), and
  2. has a heart rate > 75/min, and
  3. a left ventricular fraction < 35%
376
Q

What is the gold standard IVx to diagnose aortic dissection?

377
Q

If a patient with ?aortic dissection is unable to go for CT angio due to being unstable, what is the next best investigation?

A

Transoesophageal echo (TOE)

378
Q

What is the most common type of aortic coarctation?

A

Post-ductal - this means that the narrowing is after ductus arteriosus and hence after the subclavian artery meaning the BP in the upper limbs is greater than that of the lower limbs

Year 6 (18 decks)

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