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Year 4 > Acute Medicine > Flashcards

Acute Medicine Flashcards

1
Q

What is sepsis?

A

= where body launches a large immune response to an infection causing systemic inflammation and organ dysfunction

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2
Q

What is disseminated intravascular coagulopathy (DIC)?

A

= when coagulation system gets activated formation of clots consumes platelets and clotting factors leading to > thrombocytopenia + uncontrolled bleeding (haemorrhage)

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3
Q

What 2 things are required to diagnose septic shock?

A
  • low mean arterial pressure (below 65mmHg)
  • raised serum lactate (above 2 mmol/L)
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4
Q

What 6 parameters are measured to create NEWS2 score?

A
  • temperature
  • heart rate
  • respiration rate
  • oxygen saturations
  • blood pressure
  • consciousness level
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5
Q

In patients with suspected sepsis, within how much amount of time should they be assessed and start treatment?

A

= 1 hour of presenting

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6
Q

What 3 tests + 3 treatments make up the Sepsis 6?

A

3 tests: serum lactate, urine output, blood cultures

3 treatments: oxygen to maintain oxygen saturations, empirical broad-spectrum antibiotics + IV fluids

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7
Q

What is neutropenic sepsis?

A

= refers to sepsis in someone with a neutrophil count below 1x10^9/L

Is a life threatening medical emergency

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8
Q

Key features that differentiate anaphylaxis from non-anaphylactic allergy reaction (3)

A

Compromise of airway, breathing, or circulation

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9
Q

If patient is suffering an anaphylaxis reaction, what position is best to put the patient in?

A

= lie patient flat to improve cerebral perfusion

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10
Q

Once diagnosis of anaphylaxis is established, what 3 medications are given to treat the reaction?

A
  • IM adrenalin, repeated after 5 minutes if required
  • Antihistamines (oral Chlorphenamine, or Cetrizine)
  • Steroids (IV Hydrocortisone)
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11
Q

Anaphylaxis: what is a biphasic reaction?

A

= after a patient suffers an anaphylaxis reaction they can have a second reaction after successful treatment of the first

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12
Q

What can be measured to confirm diagnosis of anaphylaxis?

And how soon after onset must this be measured?

A

= serum mast cell try-take

within 6 hours of the event

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13
Q

What is a major burn?

A

= any burn with > 20% TBSA of partial or full-thickness burns (not including superficial burns)

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14
Q

What is an escharotomy?

A

= an emergency surgical procedure involving incising through areas of burnt skin to release the eschar and its constrictive effects, restore distal circulation, and allow adequate ventilation

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15
Q

What is the main marker of fluid balance status in a patient who has just suffered a burn?

A

= urine output

(should be maintained in adults at > 0.5ml/kg/hr)

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16
Q

What wound dressing should be used to initially dress a burn?

A

= clingfilm can be used to allow for full evaluation of burn depth, whilst minimising fluid losses from affected wounds

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17
Q

Patient presents with a burn which is painful, and appears to be dry, blanching and erythematous, what type of burn is this likely to be:

  • superficial (frist-degree)
  • superficial partial-thickness (second degree)
  • deep partial-thickness (secondary degree)
  • full thickness (third degree)
A
  • superficial (frist-degree)
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18
Q

Patient presents with a burn which is painful, and appears to be blistered, wet, blanching and erythematous, what type of burn is this likely to be:

  • superficial (frist-degree)
  • superficial partial-thickness (second degree)
  • deep partial-thickness (secondary degree)
  • full thickness (third degree)
A
  • superficial partial-thickness (second degree)
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19
Q

Patient presents with a burn which has decreased sensation, it appears yellow (or white), dry and non-blanching, what type of burn is this likely to be:

  • superficial (frist-degree)
  • superficial partial-thickness (second degree)
  • deep partial-thickness (secondary degree)
  • full thickness (third degree)
A
  • deep partial-thickness (secondary degree)
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20
Q

Patient presents with a burn which is painless, appears leathery or waxy white, is non-blanching and dry, what type of burn is this likely to be:

  • superficial (frist-degree)
  • superficial partial-thickness (second degree)
  • deep partial-thickness (secondary degree)
  • full thickness (third degree)
A
  • full thickness (third degree)
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21
Q

What is the ‘Modified Parkland Formula’ used for?

A

= acts as a guide and describes the volume of crystalloid fluid (ideally Hartmanns solution) to be administered in the first 24-hours post-burn

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22
Q

What is the ‘modified parkland formula’ for adults?

A

initial 24 hours: 4mL (Hartmann’s) x weight (kg) x %TBSA burned

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23
Q

How should the calculated volume of fluid resuscitation using the ‘modifies parkland formula’ be given?

A

= 50% given within the first 8 hours post-burn, and remaining 50% is give in the remaining 16 hours

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24
Q

What can be measured on an ABG to look for carbon monoxide poisoning?

A

= carboxyhaemoglobin levels

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25
Q

What is inhalation injury?

A

= damage to airway, secondary to inhalation of hot air

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26
Q

What is acute mesenteric ischaemia?

A

= lack of blood flow through the mesenteric vessels supplying the intestines, typically caused by rapid blockage in the blood flow through the superior mesenteric artery

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27
Q

Main risk factor in acute mesenteric ischaemia?

A

= atrial fibrillation (AF)

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28
Q

Imaging used to diagnose acute mesenteric ischaemia?

A

= contrast CT

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29
Q

Patients with acute mesenteric ischaemia will have:

  • metabolic acidosis
  • metabolic alkalosis
A
  • metabolic acidosis

(and raised lactate)

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30
Q

ACEi affect on kidneys?

A

= long-term they are kidney protective. However, stopped during AKI as they reduce filtration pressure

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31
Q

Most common intrinsic cause of AKI?

A

= acute tubular necrosis

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32
Q

What do muddy brown clasts on urinalysis suggest?

A

= acute tubular necrosis

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33
Q

NICE guidelines for diagnosing an AKI? (3)

A
  • rise in creatinine more than 25 micromol/L in 48 hours
  • rise in creatinine of more than 50% in 7 days
  • urine output of less than 0.5ml/kg/hour over at least 6 hours
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34
Q

Patient being treated for DKA develops headache, and shows altered behaviour. What should be concerned about?

A

= cerebral oedema

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35
Q

What is hypoglycaemia defined as? (value)

A

= blood glucose < 3.0 mmol/L

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36
Q

Patient is experiencing severe hypoglycaemia however, has no IV access, what is an alternative to dextrose?

A

= Glucagon IM, 1mg/kg

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37
Q

3 key features in DKA?

A
  • ketoacidosis
  • dehydration
  • potassium imbalance
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38
Q

What is thyrotoxic storm?

A

= life-threatening condition caused by an excess of thyroid hormone. Rare complication of hyperthyroidism, occurring with untreated or inadequately treated disease

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38
Q

Signs + symptoms associated with thyrotoxic storm? (3)

A
  • tachycardia
  • fever
  • altered mental status
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38
Q

What is used for symptom control in thyrotoxic storm?

A

= beta-blockers (IV Propranolol)

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39
Q

What is used to reduce thyroid activity in thyrotoxic storm?

A

= Propylthiouracil

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40
Q

What is a PE?

A

= blood clot (thrombus) in the pulmonary arteries

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41
Q

What effect can a PE have on the heart?

A

= strains the right side of the heart

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42
Q

Risk factors for a PE or DVT (VTE) (9)

A
  • Immobility
  • Recent surgery
  • Long-haul flight
  • Pregnancy
  • Hormone therapy with oestrogen (e.g., combined oral contraceptive pill or hormone replacement therapy)
  • Malignancy
  • Polycythaemia (raised Hb)
  • Systemic lupus erythematous (SLE)
  • Thrombophilia
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43
Q

What are patient’s with a high risk of developing a VTE given for prophylaxis?

A

= low molecular weight Heparin (unless contraindicated)

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44
Q

What is the PERC rule?

A

= pulmonary embolism rule-out criteria - recommended when the clinician estimates less than a 15% probability of a PE to decide whether further investigation for a PE is required

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45
Q

Criteria which make up the Wells Score for a PE

A
  • clinical signs + symptoms of a DVT (yes, +3)
  • PE is #1 diagnosis or equally likely (yes, +3)
  • HR > 100 (yes, +1.5)
  • immobilisation at least 3 days OR recent surgery in the last 4 weeks (yes, +1.5)
  • previous, objectively diagnosed PE or DVT (yes, +1.5)
  • haemoptysis (yes, +1)
  • malignancy with treatment within 6 months of palliative (yes, +1)
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46
Q

What wells score indicates a PE is likely?

A

= more than 4

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47
Q

What are the different outcomes regarding a Wells score?

A

If likely (>4): perform a CTPA, or alternative imaging

If unlikely (<4): d-dimer, if +ve perform a CTPA

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48
Q

Causes of a raised d-dimer (excluding PE) (5)

A
  • pneumonia
  • malignancy
  • HF
  • surgery
  • pregnancy
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49
Q

3 different imaging options for investigating a suspected PE?

A
  • CTPA (first-line)
  • ventilation-perfusion single photon emission computer tomography (V/Q SPECT)
  • plantar ventilation-perfusion (VQ) scan
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50
Q

What may you see on an ABG for a patient with a PE?

A

= respiratory alkalosis

(low pO2)

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51
Q

What other reasons may a patient have a respiratory alkalosis (excluding a PE)?

A

= hyperventilation syndrome

(however, patients will have a high pO2)

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52
Q

Management of PE: what is the first-line for anticoagulation?

What is the alternative?

A

= DOAC, Apixaban or Rivaroxaban

(alternative: LMWH)

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53
Q

Management of PE: When might continuous infusion of unfractionated Heparin used?

A

= massive PE with haemodynamic compromise

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54
Q

Options for long-term anticoagulation after a PE (3)

A
  • DOACs
  • Warfarin
  • LMWH
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55
Q

When might DOACs not be appropriate for long-term anticoagulation after a PE?

A
  • severe renal impairment
  • antiphospholipid syndrome
  • pregnancy
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56
Q

What can be used instead of a DOAC for long-term anticoagulation in a patient with a PE and with antiphopholipid syndrome?

A

= Warfarin

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57
Q

What can be used instead of a DOAC for long-term anticoagulation in a pregnant patient with a PE?

A

= LMWH

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58
Q

PE: How long should you continue with anticoagulation if the cause is ‘reversible’?

A

= 3 months

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59
Q

PE: How long should you continue with anticoagulation if the patient has active cancer?

A

= 3-6 months, then review

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60
Q

3 key causes of pancreatitis?

A
  • gallstones
  • alcohol
  • post-ERCP
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61
Q

Causes of pancreatitis (11)

A

Mnemonic: I GET SMASHED

I - idiopathic
G - gallstones
E - ethanol
T - trauma
S - steroids
M - mumps
A - autoimmune
S - scorpion bite
H - hypercalcaemia, hypertriglyceridemia, hypothermia
E - ERCP
D - Drugs

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62
Q

Which kind of drugs can cause acute pancreatitis?

HINT: FAT SHEEP

A

F - Furosemide
A - Azathioprine, Asparaginase
T - Thiazide, Tetracycline
S - Statins, Sulphonamides, Sodium Valproate
H - Hydrochlorothiazide
E - Estrogens, Ethanol
P - Protease inhibitors + NRTIs

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63
Q

What are Grey-Turner’s + Cullen’s sign suggestive of?

A

= haemorrhagic pancreatitis

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64
Q

What is Grey-Turner’s sign?

A

= bruising along the flanks

(suggestive of haemorrhagic pancreatitis)

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65
Q

What is Cullen’s sign?

A

= bruising around peri-umbilical area

(suggestive of haemorrhagic pancreatitis)

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66
Q

Which enzymes are important to check in suspected pancreatitis? Which is more sensitive + specific?

A
  • amylase (threefold elevation in levels)
  • lipase (more sensitive + specific)
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67
Q

What is the Glasgow Score used for?

A

= used to assess the severity of pancreatitis

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68
Q

Management of acute pancreatitis

A
  • aggressive fluid resuscitation
  • catheterisation
  • analgesia
  • anti-emetics
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69
Q

What imaging may be useful in suspected pancreatitis complications?

A

= CT abdomen

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70
Q

What is the most widely abused substance in the UK?

A

= alcohol

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71
Q

When will signs of alcohol withdrawal typically present?

(hours)

A

= 6-12 hours

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72
Q

When will signs of alcohol hallucinosis typically present?

(hours)

A

= 12-24 hours

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73
Q

When will signs of deliriums tremens typically present?

(hours)

A

= 72 hours post-drink

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74
Q

Management of delirium tremens?

A

= oral Lorazepam (parenteral Lorazepam if oral treatment refused)

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75
Q

Management in alcohol withdrawal used to prevent Wernicke’s encephalopathy?

A

= Pabrinex

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76
Q

Pharmacological management of alcohol withdrawal

A

= Chlordiazepoxide, in a reducing regime

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77
Q

What is an anastomotic leak?

A

= postoperative complication, where the contents of a hollow organ, which were surgically joined, leak through a defect in the join

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78
Q

Possible anastomotic leak complications (3)

A
  • peritonitis
  • colonic abscess formation
  • abdominal sepsis
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79
Q

How may a small anastomosis leak be managed (3)

A

Conservative management:
- bowel rest
- IV fluids
- antibiotics

(coupled with abdominal management)

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80
Q

How may a large anastomosis leak be managed (3)

A

= emergency laparoscopic exploration and potential further surgery

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81
Q

What is ascending cholangitis?

A

= severe, acute infection and inflammation of the biliary tree

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82
Q

Most common cause of ascending cholangitis?

A

= biliary calculi (stones)

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83
Q

Causes of ascending cholangitis (3)

A
  • biliary calculi (stones)
  • benign biliary strictures
  • malignancy
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84
Q

What is the Charcot’s triad made up of, and what is this suggestive of?

A
  • RUQ pain
  • fever
  • jaundice

= suggestive of ascending cholangitis

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85
Q

What is the Reynold’s triad made up of, and what is this suggestive of?

A
  • RUQ pain
  • fever
  • jaundice
  • hypotension
  • mental confusion

(Charcot’s triad + 2 more symptoms)

= suggestive of severe case of ascending cholangitis

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86
Q

First-line scan in suspected ascending cholangitis

A

= USS

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87
Q

Which scan is most accurate in determining causative disease in ascending cholangitis?

A

= MRCP

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88
Q

Management of ascending cholangitis (3)

A
  • IV fluids
  • antibiotics
  • biliary drainage

(include assessment and management of underlying cause)

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89
Q

What is disseminated intravascular coagulation (DIC)?

A

= complex condition that described the inappropriate activation of the clotting cascades, resulting in thrombus formation and subsequently leading the depletion of clotting factors and platelets

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90
Q

Type of haematological malignancy associated with DIC?

A

= sub-type of AML - acute promyelocytic leukaemia (APL)

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91
Q

Patient with DIC would have: (high or low)

  • PT time
  • APTT
  • fibrinogen
A
  • PT time - prolonged
  • APTT: increased
  • Fibrinogen: low
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92
Q

What is infectious mononucleosis also known as?

A

= glandular fever

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93
Q

Cause of glandular fever?

A

= Epstein Barr virus

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94
Q

Most prominent symptom in teenagers with glandular fever?

A

= debilitating fatigue

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95
Q

Signs and symptoms of glandular fever (4)

A
  • fever
  • sore throat
  • fatigue
  • hepatomegaly and/ or splenomegaly
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96
Q

What is the ‘Paul Bunnell’ test used to diagnose?

A

= glandular fever

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97
Q

Why is it recommended for patients with glandular fever to avoid contact sports?

A

= to minimise risk of splenic rupture

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98
Q

What is a haemorrhagic stroke?

A

= cerebrovascular event that occurs when the wall of a blood vessel in the brain weakens and ruptures

This causes bleeding in the brain, leading to haematoma formation, and consequently neuronal injury

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99
Q

Are ischaemic or haemorrhagic strokes more common?

A

= ischaemic storke

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100
Q

Are haemorrhagic strokes more common in women or men?

A

= men

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101
Q

First-line imaging used to quickly identify haemorrhagic stroke?

A

= CT scan

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102
Q

Why is BP control important in haemorrhagic stroke management?

A

= poor control in acute phase is associated with worse long-term outcomes

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103
Q

What is Horner’s syndrome?

A

= condition characterised by a set of signs and symptoms that occur due to a disruption in the sympathetic nerve supply to the eye

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104
Q

Causes of Horner’s syndrome (3)

A
  • pancoast tumour (non-small cell lung carcinoma)
  • stroke (lateral medullar infarction or Wallenberg’s syndrome)
  • carotid artery dissection
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105
Q

Young person presents with Horner’s syndrome, accompanied by neck pain - what is the likely cause?

A

= carotid artery dissection

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106
Q

Symptoms a person with Horner’s syndrome may present with? (5)

A
  • ptosis (drooping eyelid)
  • miosis (constricted pupil)
  • anhidrosis (lack of sweating on affected side of the face)
  • enophthalmos (eye appears sunken)
  • heterochromia (eye colour may change, associated with congenital Horner’s syndrome)
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107
Q

Horner’s syndrome: In pharmacological pupil testing, what occurs when OH-Amphetamine is placed in affected eye for the following:

  • pre-ganglionic cause
  • post-ganglionic cause
A

Pre-ganglionic cause: patient’s eye dilates

Post-ganglionic cause: patient’s eye will not dilate

(OH-amphetamine promotes the release of norepinephrine from the postganglionic nerve terminals)

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108
Q

Imaging used first-line to investigate hyperthyroidism

A

= USS of the thyroid

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109
Q

Antithyroid drugs used first-line in hyperthyroidism (2)

A
  • Carbimazole
  • Propylthiouracil
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109
Q

Test to help determine the cause of hyperthyroidism

A

= radioiodine uptake test

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110
Q

Which antithyroid drug is recommended for pregnant women, or those planning pregnancy?

A

= Propylthiouracil

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111
Q

Important side effect of Carbimazole

A

= agranulocytosis

Patients should be advised to seek immediate medical attention if they experience symptoms like fever, sore throat, mouth ulcers, or other signs of infection

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112
Q

What can be used for symptomatic relief in hyperthyroidism?

A

= beta-blockers (e.g., Propanolol)

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113
Q

Definitive treatment options for hyperthyroidism (2)

A
  • radio-iodine
  • surgery (thyroidectomy)
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114
Q

What is thyroid storm?

A

= rare, but life-threatening medical emergency, caused by untreated or inadequately managed hyperthyroidism

Often precipitated by stressors such as, surgery, trauma, or infection

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115
Q

Management of thyroid storm

A
  • IV Propanolol + Digoxin: for cardiac symptoms
  • Propylthiouracil through nasal gastric tube + Lugol’s iodine: to reduce thyroid hormone production
  • Prednisolone or Hydrocortisone: inhibits peripheral conversion of T4 > T3
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116
Q

What is hypothermia (°C)?

A

= defined as core body temperature of < 35°C

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117
Q

What is severe hypothermia defined as?

A

= < 28°C

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118
Q

Patient presents with tachycardia, tachypnoea, vasoconstriction, and shivering, after being found outside on a cold winters day.

They have a temperature of 33°C

Which of the following types of hypothermia does this patient most likely have?

  • mild hyperthermia
  • moderate hyperthermia
  • severe hyperthermia
A
  • mild hyperthermia
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119
Q

Patient presents with cardiac arrhythmia, hypotension, respiratory depression, reduced consciousness and is not shivering, after being found outside on a cold winters day.

They have a temperature of 30°C

Which of the following types of hypothermia does this patient most likely have?

  • mild hyperthermia
  • moderate hyperthermia
  • severe hyperthermia
A
  • moderate hyperthermia
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120
Q

Patient presents with marked reduced consciousness/ coma, apnoea, arrhythmia with fixed dilated pupils, after being found outside on a cold winters day.

They have a temperature of 27°C

Which of the following types of hypothermia does this patient most likely have?

  • mild hyperthermia
  • moderate hyperthermia
  • severe hyperthermia
A
  • severe hyperthermia
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121
Q

The following ECG features are suggestive of?

  • bradyarrhythmia
  • Osborne waves (‘J’ waves)
  • prolonged PR, QRS, and QT intervals
  • ventricular ectopics
  • cardiac arrest
A

= hypothermia

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122
Q

What are Osborne waves (‘J’ waves) pathognomonic for?

A

= hypothermia

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123
Q

What do ‘J waves’ look like on an ECG?

A

= positive deflection at the J point between the end of the QRS complex and beginning of the ST segment

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124
Q

What medical emergency are patients with hypothermia at risk of?

A

= cardiac arrest

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125
Q

What are Osborne waves on an ECG also known as?

A

‘J waves’

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126
Q

What is idiopathic intracranial hypertension?

A

= disorder of unidentifiable cause which leads to increased intracranial pressure

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127
Q

What opening pressure on lumbar puncture insinuate idiopathic intracranial hypertension?

A

= above 25 cmH2O

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128
Q

Is idiopathic intracranial pressure more common in women or males?

A

= usually more common in young + obese women

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129
Q

Which drugs are associated with raised intracranial pressure? (5)

A
  • oral contraceptive pill
  • steroids
  • tetracycline
  • vitamin A
  • lithium
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130
Q

What may be seen on ophthalmoscopy in patient with idiopathic intracranial pressure?

A

= bilateral papilloedema

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131
Q

Key diagnostic tool in idiopathic intracranial hypertension

A

= lumbar puncture

(revealing an opening pressure above 20 cmH2O)

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132
Q

First-line management for idiopathic intracranial hypertension

A

= weight loss

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133
Q

First-line analgesia for patients with major trauma?

A

= IV morphine

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134
Q

Causative organism in meningococcal infection?

A

= Neisseria meningitides bacterium

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135
Q

Where does Neisseria meningitidis bacterium usually reside?

A

= nasopharynx of many children and young adults

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136
Q

How is meningococcal infection transmitted?

A

= via respiratory droplet spread

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137
Q

What is Waterhouse-Friderichsen Syndrome? and what disease is this associated with?

A

= a rare but life-threatening disorder associated with bilateral adrenal hemorrhage

In many cases, it is caused by fulminant meningococcemia (associated with meningococcal infection)

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138
Q

How is meningococcal infection diagnosed? (2)

A

= blood cultures, or CSF (where appropriate)

PCR also highly sensitive + another key investigative tool

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139
Q

Management in suspected meningococcal infection

A

Early antibiotic treatment (broad-spectrum IV), until pathogen identified

Abx adjusted to penicillin-based treatment

Notifiable disease - contact public health authorities

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140
Q

Meningococcal infection: for all household, or close contacts, what can be given as post-exposure prophylaxis?

A

= Ciprofloxacin or Rifampicin

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141
Q

Is meningococcal infection a notifiable disease?

A

= yes, need to contact the public health authorities

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142
Q

What is myxoedema coma?

A

= aka, severe decompensated hypothyroidism - most severe form of hypothyroidism

Typically triggered by an acute event such as infection, MI or drug use

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143
Q

Primary cause of myxoedema coma

A

= severe or untreated hypothyroidism

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144
Q

Signs and symptoms of myxoedema coma (7)

A
  • profound lethargy or coma
  • hypothermia
  • bradycardia + hypotension
  • hypoventilation
  • hypoglycaemia
  • hyponatraemia
  • generalised myxoedema
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145
Q

What is seen in patients in a myxoedema coma:

  • hyperventilation
  • hypoventilation
A
  • hypoventilation
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146
Q

Management of myxoedema coma (5)

A
  • IV T3/T4
  • 50-100mg IV Hydrocortisone
  • Oxygen + mechanical ventilation
  • IV fluids
  • correction of hypothermia, hypoglycaemia + treatment of many HF
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147
Q

What is necrotising fasciitis?

A

= severe life-threatening infection characterised by rapidly progressing inflammation and necrosis of the fascia and subcutaneous tissue

While it spreads along the fascial planes, it typically spares the underlying muscle

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148
Q

Common causative organism of necrotising fasciitis

A

= group A Streptococcus

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149
Q

What gas-forming organism can cause necrotising fasciitis?

(causes type III NF)

A

= Clostridium perfringens

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150
Q

What is Fournier’s gangrene?

A

= necrosis fasciitis of the perineum

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151
Q

Who is at a higher risk of developing Fournier’s gangrene?

(taking what medication)

A

= diabetics taking SGLT-2 inhibitors (-gliflozins)

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152
Q

3 types of necrotising fascinating

A

Type 1: poly microbial
Type 2: mono microbial (typically caused by Group A Streptococcus, or Staphylococci)
Type 3: often caused by gas-forming organisms, such as Clostridium perfringens, leading to ‘gas gangrene’

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153
Q

Management of necrotising fasciitis (2)

A
  • urgent surgical debridement
  • broad-spectrum antibiotic therapy (IV Clindamycin, Meropenem, and Vancomycin)
  • haemodynamic support (IV fluids, vasopressors, and supportive care)
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154
Q

What is oesophagitis?

A

= inflammation of the oesophagus

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155
Q

Most common cause of oesophagitis?

A

= reflux of gastric contents

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156
Q

Investigation for oesophagitis (2)

A
  • endoscopy: allows for direct visualisation, grading + allows biopsy
  • oesophageal pH monitoring: to help determine whether symptoms timing and reflux correlate
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157
Q

Pharmacological treatment for oesophagitis

A

= full-dose PPI for 1 month

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158
Q

How long should a patient with oesophagitis be on PPIs?

A

= 1 month

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159
Q

Lifestyle changes which should be advised to patients with oesophagitis (3)

A
  • weight loss
  • cessation of smoking
  • reduction in alcohol intake
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160
Q

What is a compound fracture?

A

= AKA open fracture, is a type of bone fracture characterised by a breach in the skin that allows the fractured bone to communicate directly with the outside environment

This exposes the injury site to potential contaminants, thereby increasing the risk of infection

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161
Q

Acetaminophen is also known as?

A

= Paracetamol

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162
Q

Most common agent for intentional self-harm in the UK?

A

= paracetamol overdose

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163
Q

Pathophysiology of paracetamol overdose

A

= normally, NAPQI is inactivated by glutathione, but during an overdose, glutathione stores are rapidly depleted, leaving NAPQI unmetabolised and resulting in liver and kidney damage

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164
Q

What is the toxic substance which builds-up in a paracetamol overdose?

A

= N-acetyl-p-benzoquinone-imine (NAPQI)

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165
Q

Patient comes in following a paracetamol overdose, ingestion < 1 hour ago + dose > 150mg/kg

What do you do?

  • Administer activated charcoal
  • Treat with N-acetylcysteine
  • Wait 4 hours to take level, then treat with N-acetylcystine
A
  • Administer activated charcoal
166
Q

Patient comes in following a paracetamol overdose, ingestion < 4 hour ago

What do you do?

  • Administer activated charcoal
  • Treat with N-acetylcysteine
  • Wait 4 hours to take level, then treat with N-acetylcystine
A
  • Wait 4 hours to take level, then treat with N-acetylcystine
167
Q

Patient comes in following a paracetamol overdose, ingestion within 4-8 hours ago + dose > 150mg/kg

What do you do?

  • Administer activated charcoal
  • Treat with N-acetylcysteine
  • Wait 4 hours to take level, then treat with N-acetylcystine
A
  • Treat with N-acetylcysteine

(immediately if there is going to be a delay of >/= 8 hours in obtaining paracetamol level

168
Q

Patient comes in following a paracetamol overdose, ingestion > 24 hours ago

What do you do?

  • Administer activated charcoal
  • Treat with N-acetylcysteine
  • Wait 4 hours to take level, then treat with N-acetylcystine
A
  • Treat with N-acetylcysteine
169
Q

Patient comes in following a staggered paracetamol overdose

What do you do?

  • Administer activated charcoal
  • Treat with N-acetylcysteine
  • Wait 4 hours to take level, then treat with N-acetylcystine
A
  • Treat with N-acetylcysteine
170
Q

What is King’s College Criteria used for in paracetamol overdose? (2)

A

= used to predict mortality from paracetamol overdose

And to identify those patients who would potentially benefit from liver transplantation

171
Q

What occurs in an acute aortic thoracic dissection?

A

= occurs when a tear in the tunica intima of the aorta creating a false lumen whereby blood can flow between the inner and outer layers of the walls of the aorta

172
Q

Risk factors of aortic dissection (4)

A
  • hypertension
  • connective tissue disease (e.g., Marfan’s syndrome)
  • valvular heart disease
  • cocaine/ amphetamine use
173
Q

Stanford Classifications of aortic dissections (type A + B)

A

Stanford type A: involves ascending aorta, arch of the aorta

Stanford type B: involves the descending aorta

174
Q

Are aortic dissections more common in men or women?

A

= men

175
Q

What is radio-radial delay?

(clinical sign)

A

= loss of synchronicity between the radial pulse on each arm, resulting in the pulses occurring at different time

176
Q

Key investigation in diagnosing aortic dissection?

A

= CT angiogram

177
Q

Aortic dissection, what is used to control BP?

A

= IV Metoprolol infusion

178
Q

Definitive management options for both type A and B aortic dissections

A

Type A: usually requires surgical management (e.g., aortic graft)

Type B: normally managed conservatively with BP control

179
Q

What is cardiac syncope?

A

= transient loss of consciousness as a result of inadequate cardiac output leading to cerebral hypoperfusion

180
Q

Patient presents following collapse, seen to be found exertion syncope. What do you make of this?

A

= suggests cardiac cause

Exertional syncope is a red flag symptom and warrants serious investigation

181
Q

Imaging which can be used to look for structural causes of cardiac syncope

A

= trans-thoracic echocardiogram (TTE)

182
Q

DVLA advice if patient suffers an unexplained syncope

A

= 6 months off driving and need to inform the DVLA

183
Q

What is serotonin syndrome?

A

= potential life-threatening condition resulting from increased serotoninergic activity within the CNS

184
Q

Triad of clinical features seen in patients with serotonin syndrome

A
  • mental status changes
  • autonomic hyperactivity
  • neuromuscular abnormalities
185
Q

What is Cyproheptadine used for?

A

= is an antidote for serotonin syndrome

186
Q

Types of shock and what causes them (6)

A
  • Hypovolaemic: due to blood loss
  • Septic: from severe systemic infection
  • Anaphylactic: allergic reaction
  • Cardiogenic: poor cardiac output
  • Neurogenic: caused by damage to the nervous system
  • Obstructive: caused by physical obstruction to vessels or the heart
187
Q

Management of traumatic shock (hypovolaemia) (2)

A
  • administer 1.5-2L warmed IV crystalloid, assess for response
  • if inadequate response to fluid, arrange 0-negative blood. Give fully cross-matched blood as soon as possible
188
Q

What is a space occupying lesion?

A

= refers to any pathological entity, such as tumours or abscesses, that occupy space within the cranial vault

189
Q

Describe pathophysiology of Cushing’s reflex

A

Is a response to raised intracranial pressure. This results in reduced cerebral perfusion and so the resultant cerebral ischaemia, causes massive sympathetic activation (Cushing’s reflex)

190
Q

Triad of Cushing’s reflex

A
  • bradycardia
  • irregular respirations
  • high systolic BP (widened pulse pressures)
191
Q

Initial imaging in acute setting where space-occupying lesion is suspected

A

= CT head

192
Q

What is the Glasgow coma scale (GCS)?

A

= universal score used in the assessment of conscious level of a patient

193
Q

Minimum score you can get on the GCS scale?

A

= 3

194
Q

What does a GCS < 8 signify?

A

= suggests that patient is unable to maintain their own airway adequately, and warrants urgent assessment by the anaesthetic team

195
Q

ECG finding, seen in person with tricyclic antidepressant overdose

A

= QT interval prolongation

196
Q

What is given to treat TCA overdose?

A

= IV Sodium Bicarbonate

(if presents within 2-4 hours of overdose, consider activated charcoal)

197
Q

What is Wolff-Parkinson-White Syndrome?

A

= congenital pre-excitation syndrome that occurs due to the presence of an accessory electrical pathway between the atria and ventricles

198
Q

What arrhythmia does Wolff-Parkinson-White syndrome predispose you to?

A

= supraventricular tachycardias

199
Q

Is wolff-parkinson-white syndrome more common in men or women?

A

= men

200
Q

Which of the following is Type A vs Type B Wolff-Parkinson-White Syndrome

  • pathway between L atrium + ventricle
  • pathway between R atrium + ventricle
A

Type A: pathway between L atrium + ventricle

Type B: pathway between R atrium + ventricle

201
Q

First-line investigation in patient with Wolff-Parkinson-White syndrome you can do bedside?

A

= ECG

202
Q

In what condition do you see the following ECG changes:

  • delta waves
  • short PR interval
  • broadened QRS complex
A

= wolff-parkinson-white syndrome

203
Q

Anti-arrhythmic used in long-term management of wolff-parkinson-white syndrome (2)

A
  • Amiodarone
  • Sotalol
204
Q

Amiodarone + Sotalol (anti-arrhythmics) are contraindicated in patients with…?

A

= structural heart disease

205
Q

Definitive management of Wolff-parkinson-white syndrome

A

= radio frequency ablation (or open-heart performed in complex cases)

206
Q

Patient with wolff-parkinson white presents with tachyarrhythmia

If there are adverse signs such as shock, syncope, HF, or myocardial ischaemia, what is first-line management?

A

= synchronised DC cardioversion

207
Q

Patient with wolff-parkinson white presents with tachyarrhythmia

If patient is stable but presenting with a narrow complex tachycardia with short PR intervals, what is the first + second-line management?

A

First-line: vagal manoeuvres

Second-line: Adenosine

208
Q

Success rate of WPW syndrome being treated with ablation

A

= high, 95% success rate

209
Q

What is primary angle closure glaucoma (PACG)?

A

= type of glaucoma characterised by the blockage or narrowing of the drainage angle formed by the cornea and iris, resulting in sudden increase in intraocular pressure

210
Q

Risk factors for developing angle closure glaucoma (4)

A
  • hyperopia (long-sightedness) and short axial length of eyeball
  • age
  • ethnicity: Inuit or Asian population
  • pupillary dilation (iatrogenically or environmental)
211
Q

What is hyperopia?

A

= long-sightedness

212
Q

What do the following symptoms suggest:

  • painful eye that develops rapidly
  • eyes appear red, ciliary flush with hazy cornea
  • burred vision
  • systemically unwell
  • patient desired seeing haloes around lights
  • raised IOP detected
A

= acute angle closure glaucoma

213
Q

Definitive management of acute angle closure glaucoma

A

= peripheral iridotomy

214
Q

What is peripheral iridotomy?

A

= laser used to make hole in the peripheral iris to allow free flow of aqueous

(definitive treatment for acute angle closure glaucoma)

215
Q

IOP-lowering agents (3)

A
  • beta-blockers
  • Pilocarpine
  • IV acetazolamide
216
Q

Which of the following peak expiratory flow readings suggests moderate asthma in an acute attack?

  • PEF >50-75%
  • PEF >35-50%
  • PEF 33-50%
  • PEF < 35%
  • PEF < 33%
A
  • PEF >50-75%
217
Q

Which of the following peak expiratory flow readings suggests severe asthma in an acute attack?

  • PEF >50-75%
  • PEF >35-50%
  • PEF 33-50%
  • PEF < 35%
  • PEF < 33%
A
  • PEF 33-50%
218
Q

Which of the following peak expiratory flow readings suggests life-threatening asthma in an acute attack?

  • PEF >50-75%
  • PEF >35-50%
  • PEF 33-50%
  • PEF < 35%
  • PEF < 33%
A
  • PEF < 33%
219
Q

Why might patients with life-threatening asthma have a normal PCO2, between 4.6-6.0?

A

= unable to ventilate appropriately (as you’d expect this group to have low PCO2 level)

220
Q

What is raised PCO2 a sign of, in an acute asthma attack?

A

= near-fatal sign of asthma

221
Q

Immediate management of an acute asthma attack (4)

A
  1. sit-up
  2. 100% O2 via non-rebreathe mask (aim for 94-98%)
  3. Nebulised Salbutamol (5mg) +/- Ipratropium (0.5mg) depending on response to Salbutamol
  4. Hydrocortisone 100mg IV, or Prednisolone 50mg PO
222
Q

Life-threatening asthma attack management (3)

A
  • inform intensive care team
  • Magnesium sulphate 2g IV over 20 minutes
  • Nebulised Salbutamol every 15 minutes
223
Q

3 things to keep an eye on whilst monitoring a patient who presented with acute asthma attack

A
  • peak flow (every 15 minutes, pre- and post-Salbutamol)
  • SpO2
  • ABG measurements
224
Q

How Is unstable angina differentiated from NSTEMI?

A

Unstable angina: no rise in troponin

NSTEMI: rise in troponin

225
Q

How is STEMI differentiated from NSTEMI?

A

= ECG changes

STEMI: ST-elevation, or LBBB
NSTEMI: new ST-depression, T-wave inversion

226
Q

Which type of patients are more likely to experience a ‘painless’ MI (2)

A

= diabetics, and older patients

227
Q

Initial treatment of STEMI

‘MMONAC’

A

M - Morphine
M - Metoclopramide
O - Oxygen
N - Nitrates (GTN spray)
A - Aspirin 300mg
C - Clopidogrel 300mg

228
Q

Patient admitted with STEMI, has presented within 12 hours of symptoms onset, and within 2 hours of medical contact.

What procedure is most appropriate?

A

= PCI

229
Q

Patient admitted with STEMI, has presented within 12 hours of symptoms onset, but after 2 hours of medical contact.

What procedure is most appropriate?

A

= thrombolysis

230
Q

What can be offered to patients with NSTEMI who are deemed high risk of death and further ischaemic events - if presented within 12-24 hours?

A

= re-vascularisation

231
Q

What oxygen should be given to a patient experiencing an acute exacerbation of COPD

A

= 24% O2 via Venturi mask

(SpO2: 88-92%)

232
Q

In patient experiencing an acute exacerbation of COPD, what should be considered if their pH<7.26?

A

= invasive intervention

233
Q

What non-invasive ventilation can be used in patients’s suffering an acute exacerbation of COPD?

A

= BiPAP (bilevel positive airway pressure)

234
Q

What is acute pulmonary oedema?

A

= accumulation of excess fluid in the pulmonary system, particularly within the lung parenchyma and alveoli

235
Q

What is an open book pelvis?

A

= fracture of the pubic rami with a posterior pelvic disruption of the sacro-iliac joint

236
Q

Treatment of acute pulmonary oedema

A
  • position patient upright
  • administer oxygen
  • IV Furosemide

Consider non-invasive ventilation

237
Q

In patients with HF and renal impairment, would diuresis help or worsen the situation?

A

= under-perfusion likely due to poor output from the heart and therefore, by off-loading fluid with diuresis, SV improves and perfusion to kidneys improve

238
Q

Potential option in patients with acute pulmonary oedema on a background of HF, persistent hypotension, and evidence of end-organ perfusion?

A

= Vasopressors

239
Q

What is ethylene glycol found in?

A

= anti-freeze

240
Q

Management options in ethylene glycol poisoning?

A
  • gastric lavage (stomach pump), or NG aspiration (if < 1 hour since ingestion)
  • Fomepizole (prevents metabolism of ethylene glycol into toxic metabolites)
  • haemofiltration can be used in severe cases to remove toxic metabolites from the blood
241
Q

What is Fomepizole used for?

A

= antidote used in ethylene glycol poisoning (anti-freeze)

242
Q

Which of the following would you see in someone with ethylene glycol poisoning?

  • normal anion gap metabolic acidosis
  • raised anion gap metabolic acidosis
  • normal anion gap metabolic alkalosis
  • raised anion gap metabolic alkalosis
A
  • raised anion gap metabolic acidosis
243
Q

What is pericarditis?

A

= inflammation of the pericardium which is 2 layers of tissue that surround the heart

244
Q

Important to test to do in someone with suspected pericarditis?

A

= ECG

245
Q

What ECG findings suggest pericarditis? (2)

A
  • PR depression
  • global saddle-shaped ST elevation
246
Q

Emergency management of pericarditis

A

= analgesia (NSAIDs) + bed rest

(Colchicine + steroids may be used if necessary. Must also treat underlying cause)

247
Q

What is a pneumothorax?

A

= presence of air within the pleural space

248
Q

Which patients are at a higher risk of developing a spontaneous primary pneumothorax?

A

= tall, thin, young men

249
Q

Management of a primary pneumothorax if rim of air < 2cm AND patient NOT SOB

A

= consider discharge

250
Q

Management of a primary pneumothorax if rim of air < 2cm AND patient is SOB

A

= needle aspiration

251
Q

Management of a primary pneumothorax if rim of air > 2cm AND patient is still SOB

A

= chest drain

252
Q

Management of a secondary pneumothorax if rim of air is between 1-2cm?

A

= needle aspiration

253
Q

Management of a secondary patient > 50 + rim of air > 2cm, and/ OR patient is SOB?

A

= insert chest drain

254
Q

Signs of a tension pneumothorax (compared to simple pneumothorax) (2)

A
  • haemodynamic instability
  • mediastinal shift
255
Q
A
256
Q

How is a tension pneumothorax diagnosed?

A

= should be a clinically diagnosis

257
Q

Management of a tension pneumothorax

A

= immediate needle decompression using a large-bore needle (2nd intercostal space, mid-clavicular line)

Insert chest drain to prevent immediate recurrence of the tension pneumothorax

258
Q

What is encephalitis?

A

= inflammation of the brain parenchyma, aka the encephalon

259
Q

Most common cause of encephalitis?

A

= herpes simplex virus type I (viral)

260
Q

What should be suspected in a patient presenting with sudden onset behavioural changes, new seizures, and unexplained acute headache accompanied by meningism?

A

= encephalitis

261
Q

What are the triad of symptoms of meningism?

A
  • nuchal rigidity
  • photophobia
  • headache
262
Q

Herpes simplex virus encephalitis affects which lobe in the brain more commonly?

A

= temporal lobes

263
Q

Management of suspected encephalitis (2)

A
  • broad-spectrum antimicrobial cover with 2g IV Ceftriaxone BD
  • 10mg/kg Acyclovir TDS for 2 weeks (anti-viral)
264
Q

What is hyperosmolar hyperglycaemic state?

A

= serious complications of type II diabetes (T2DM), characterised by severe hyperglycaemia, hypotension and hyperosmolarity without significant ketosis or acidosis

265
Q

Diagnostic criteria for hyperosmolar hyperglycaemic state (3)

A
  • severe hyperglycaemia (>/= 30 mmol/L)
  • hypotension
  • hyperosmolarity (usually, > 320 mismos/kg)
266
Q

Management of hyperosmolar hyperglycaemic state (3)

A
  • fluid resuscitation with 0.9% saline
  • insulin at 0.05 units/kg/hour, only if ketones > 1 mmol/L or if glucose fails to fall
  • VTE prophylaxis
267
Q

Patients with hyperosmolar hyperglycaemic state are at higher risk of what?

A

= venous thromboembolism (VTE)

268
Q

What is addisonian crisis?

A

= characterised by body’s inability to produce a sufficient amount of cortisol

269
Q

What would you expect to sodium, potassium and glucose levels in addisonian crisis?

A

Sodium - low
Potassium - high
Glucose - low

270
Q

Test to confirm diagnosis of addisonian crisis?

A

= ACTH (short synacthen) test

271
Q

Management of addisonian crisis (3)

A
  • fluid resuscitation
  • IV Hydrocortisone 100mg
  • IV glucose is hypoglycaemic
  • consider Fludrocortisone if there is adrenal disease present

(transition back to oral steroids after 3 days)

272
Q

What oxygen saturations would you expect in a patient with carbon monoxide poisoning?

A

= 100% (saturation probe cannot distinguish between oxygenated + carboxyhemoglobin bound to Hb)

273
Q

Patient presents with confusion, nausea + vomiting, tachycardia + cherry red skin. Oxygen saturations are 98%.

What do you suspect is going on here?

A

= carbon monoxide poisoning

274
Q

How do you diagnose CO poisoning?

A

= venous or arterial blood gas - carboxyhemoglobin concentration > 20% is diagnostic

275
Q

Management of CO poisoning

A
  • administer 100% oxygen via non-rebreathe mask
  • hyperbaric oxygen therapy (gold-standard)
276
Q

What is hyperbaric oxygen therapy used to treat?

A

= carbon monoxide poisoning

277
Q

Electrolyte imbalance which puts you at an increased risk of digoxin toxicity?

A

= hypokalaemia

278
Q

Which kind of toxicity can cause vision with a yellow-green tint?

A

= digoxin toxicity

279
Q

Why are people with hypokalaemia more at risk of digoxin toxicity?

A

=because digoxin binds to the K+ site of the Na+/K+-ATPase pump, low serum potassium levels increase the risk of digoxin toxicity

Conversely, hyperkalemia diminishes digoxin’s effectiveness

280
Q

What is digibind used for?

A

= antidote used in digoxin toxicity

281
Q

What type of hypersensitivity reaction is anaphylaxis?

A

= severe type 1 IgE-mediated hypersensitivity reaction

282
Q

What can be measured to confirm an anaphylaxis reaction? (after patient stabilised)

A

= serum levels of mast cell tryptase

283
Q

Immediate management of patient presenting with anaphylaxis

A
  • ABCDE approach
  • oxygen
  • lay flat, legs up
  • administer Adrenaline IM 500 micrograms (for adult)
  • if no response after 5 minutes, repeat IM adrenaline + IV fluid bolus
284
Q

What should be given to patient who presented with anaphylaxis and has been stabilised with IM adrenaline? (2)

A

= Chlorphenamine (antihistamine) + Hydrocortisone

285
Q

What is a biphasic anaphylactic response?

A

= describes the recurrence of anaphylaxis symptoms soon after the initial episode.
Occurs in 5% of cases

286
Q

If 2 doses of IM adrenaline have been given, what is the minimum time patient must be observed for?

A

= minimum 6 hours

287
Q

What makes up Beck’s triad?

A
  • raised JVP
  • hypotension
  • muffled heart sounds
288
Q

What is Kussmaul’s sign?

A

= paradoxical rise in JVP during inspiration

289
Q

What is pulsus paradoxus?

A

= decrease in systolic BP by > 10mmHg during inspiration

290
Q

Diagnostic imaging used to diagnose cardiac tamponade

A

= echocardiogram

291
Q

Treatment for cardiac tamponade

A

= pericardiocentesis

292
Q

What ECG findings can be seen in cardiac tamponade?

A

= electrical alternans

(non-specific but suggestive of tamponade)

293
Q

What is electrical alternates on ECG?

A

= alternating height of QRS complexes

294
Q

ECG shows: polymorphic VT that twists around isoelectric line + QT prolongation (> 460ms)

A

= torsades de pointes

295
Q

Initial management of patient with torsades de pointes, if patient haemodynamically unstable?

A

= DC cardioversion

296
Q

Initial management of patient with torsades de pointes, if patient haemodynamically stable?

A

= 2mg IV Magnesium Sulphate over 1-2 minutes

297
Q

1st line long-term treatment in patients with torsades de pointes with congenital LQTS?

A

= beta-blockers

298
Q

What may be considered to stop patient’s with torsades de pointes from having further episodes?

A

= inserting an implantable cardioverter defibrillator (ICD)

299
Q

Which arrhythmia increases a patients risk of developing torsades de pointes?

A

= long QT syndrome (LQTS)

300
Q

What is a broad complex tachycardia characterised as?

(HR + QRS width)

A
  • HR > 100bpm
  • QRS width > 120
301
Q

Electrolyte abnormalities which may cause ventricular tachycardia?

(K + Mg)

A

= hypokalaemia + hypomagnesaemia

302
Q

Main medical treatment option for stable patients with a regular broad complex tachycardia

A

= IV Amiodarone

303
Q

Drugs that cause QT prolongation (2)

A
  • Clarithromycin
  • Erythromycin
304
Q

Can you use Adenosine in people with asthma?

A

= no

305
Q

What can be used as an alternative to Adenosine in patients with asthma?

A

= Verapamil

306
Q

What is important to mention to a patient before they are given Adenosine?

A

= warn patient they may experience difficulty breathing, chest tightness and flushing

307
Q

What is status epilepticus defined as?

A
  • single seizure lasting > 5 minutes
  • > /= 2 seizures within 5 minutes, without person returning to normal between them
308
Q

Reversible causes which should be initially checked in a patient who is seizing (2)

A
  • blood sugar levels
  • oxygen saturations
309
Q

In pre-hospital setting what may be given initially in status epilepticus (2 + doses)

A
  • buccal Midazolam (10mg)
  • PR Diazepam (10mg)
310
Q

In hospital what is given initially to treat status epilepticus? (+dose)

A

= IV Lorazepam (4mg)

311
Q

Patient presents with status epilepticus and is treated with 4mg Lorazepam IV, what is the next step if seizure activity does not cease?

A

= repeat IV Lorazepam (4mg) after 5-10 minutes

312
Q

Patient presents with status epilepticus and is treated with 4mg Lorazepam IV, this is then repeated. What is the next step if seizure activity does not cease?

A

= add a second-line agent - Levetiracetam

313
Q

Status epilepticus: if no response to treatment within 45 minutes from onset, what options should be considered? (2)

A
  • induction of general anaesthesia
  • phenobarbital
314
Q

What is a deep vein thrombosis?

A

= refers to intra-luminal occlusion of any vein within the deep system of a limb (either arm or leg) or the pelvis

315
Q

Causes and risk factors for a DVT

(‘THROMBOSIS’)

A

T – trauma, thrombophilia
H – hormonal (COPD, pregnancy, HRT)
R – relatives (Fhx of VTE), recent surgery (orthopaedic/ pelvic in particular)
O – old (age > 60), obesity
M - malignancy
B – bone fractures
O – obesity
S - smoking
I – immobilisation (long distance travel, or recent surgery)
S - sickness

316
Q

How far below the tibial tuberosity should a calf circumference be measured in suspected DVT?

A

= 10cm below

317
Q

When measuring calf circumference in patient with suspected DVT, what difference between the 2 legs increases the probability of a DVT?

A

= > 3cm

318
Q

For which kind of patients should you arrange a same-day assessment and management if DVT is suspected?

A

= pregnant women or if has given birth within the past 6 weeks

319
Q

Non-pregnant patient is suspected of having a DVT, how can the probability be calculated?

A

= 2-level Well’s score

320
Q

What score on the 2-level Well’s scoring system makes a DVT ‘likely’?

A

= 2 points or more

321
Q

If a DVT is ‘likely’ on the Well’s score, what is the next step?

A
  • primal leg vein USS scan within 4 hours, if NOT possible,
  • d-dimer should be performed + interim anticoagulation should be administered
322
Q

DVT: what do you do if USS scan is negative, but d-dimer comes back as positive?

A

= stop interim anticoagulation and offer repeat USS 6-8 days later

322
Q

What anticoagulation is used in management of a DVT?

A

DOAC (such as Apixaban or Rivaroxaban)

(other options Warfarin, LMWH, unfractionated Heparin)

322
Q

Target INR in those taking Warfarin?

A

= INR between 2-3

322
Q

What can be used as interim anticoagulation in patient with suspected DVT?

A

= low-molecular weight heparin

(or NICE update can use anticoagulant you wish to continue with such as DOAC)

322
Q

What do you do if DVT is ‘unlikely’ on Well’s score?

A

= d-dimer test (within 4 hours)

323
Q

How long should a patient be on anticoagulation if they have a ‘provoked’ DVT?

A

= 3 months

324
Q

How long should a patient be on anticoagulation if they have a ‘unprovoked’ DVT?

A

= 6 months

325
Q

DVT: How long should a patient be on anticoagulation if they have non-modifiable risk factors?

A

= lifelong

326
Q

DVT: How long should a patient be on anticoagulation if they have an active cancer?

A

= 3-6 months

327
Q

What is an extradural haemorrhage?

(where does blood collect, which vessel is often implicated?)

A

= blood collects between dura mater (outmost meningeal layer), and surface of skull

Middle meningeal artery often implicated

328
Q

Extradural haemorrhage is common in which kind of patients?

A

= young patients who have experienced a head injury

329
Q

Scan of choice used to investigate an extradural haemorrhage

A

= CT scan

330
Q

18 y.o. patient was involved in a road traffic accident and has a headache. CT scan shows biconvex hyper dense extra-axial collection

What is the diagnosis?

A

= extradural haemorrhage

331
Q

Management options for an extradural haemorrhage (mild + severe) (2)

A

Mild: conservative treatment + close observation

Severe: urgent neurosurgical evaluation

332
Q

Signs of an upper GI bleed (2)

A
  • haematemesis (coffee-ground like)
  • Malena (black, tarry stool)
333
Q

Upper GI bleed: which of the followings signs suggests < 15% blood volume loss?

  • resting tachycardia
  • orthostatic hypertension
  • supine hypotension
A
  • resting tachycardia
334
Q

Upper GI bleed: which of the followings signs suggests at least 15% blood volume loss ?

  • resting tachycardia
  • orthostatic hypertension
  • supine hypotension
A
  • orthostatic hypertension
335
Q

Upper GI bleed: which of the followings signs suggests over 40% blood volume loss ?

  • resting tachycardia
  • orthostatic hypertension
  • supine hypotension
A
  • supine hypotension
336
Q

What is used in an upper GI bleed to reduce portal hypertension?

A

= IV Terlipressin

337
Q

What is the Glasgow-Blatchford Score used for?

A

= used in upper GI bleed - risk scoring tool used to predict need to treat in patients with an endoscopy

338
Q

How to manage an upper GI bleed?

A
  • ABCDE approach
  • stabilise patient, may require blood transfusion or FFP + platelet transfusions
  • Terlipressin - reduce portal hypertension
  • Broad spectrum antibiotics
  • urgent endoscopy
339
Q

What is the treatment of choice for a variceal bleed at endoscopy?

A

= variceal band ligation

340
Q

What is a Sengstaken-Blakemore tube? And when may it be used?

A

= used in variceal bleed if its uncontrollable. Tube inserted as a temporary measure to tamponade the bleeding variceal

341
Q

Pharmacological prevention of variceal bleeds?

A

= Propranolol (non-selective beta-blockers)

342
Q

Patient is found to have liver cirrhosis, what is important to screen for? and how is it done?

A

= important to screen for oesophageal varices, using endoscopy

343
Q

If patient with liver cirrhosis has no signs of oesophageal varices on diagnosis, when do you repeat endoscopy? if ever?

A

= after 2-3 years

344
Q

Endoscopic prevention of variceal bleeds?

A

= variceal band ligation

345
Q

Where Propranolol and band ligation fails to prevent variceal bleeds, what can be used?

A

= TIPSS (transjugular intrahepatic portosystemic shunt)

346
Q

What is The Rockall Score, and what is it used for?

A

= used in upper GI bleeds - risk assessment tool that predicts mortality in these patients

347
Q

What is bradycardia defined as?

A

= HR < 60

348
Q

Most common medications used to increase ventricular rate (used in bradycardia) (3)

A
  • IV Atropine
  • Epinephrine
  • Dopamine
349
Q

If medical therapy does not work at increased ventricular rate in bradycardia, what can be used?

A

= temporary pacing (transcutaneous + transvenous)

350
Q

Name 2 non-shockable rhythms

A
  • pulseless electrical activity
  • asystole
351
Q

What is pulseless electrical activity?

A

= where the ECG shows electrical activity that should produce a pulse, but cardiac output is absent, or insufficient, such that a pulse is not clinically detectable

352
Q

What asystole?

A

= cardiac arrest rhythm which no discernible electrical activity on the ECG monitor

353
Q

ALS: Management of pulseless electrical activity (PEA) OR asystole

A

= commence CPR immediately

Adrenaline 1mg IV given in 1st cycle + if persists, every other cycle
(e.g., cycle 1, 3, 5 etc.)

[these are non-shockable rhythms]

354
Q

Name 2 types of shockable rhythms

A
  • pulseless ventricular tachycardia
  • ventricular fibrillation
355
Q

Which rhythm presents as a broad complex tachycardia on cardiac monitoring?

A

= ventricular tachycardia

356
Q

Which rhythm presents as a chaotic irregular deflections of varying amplitude?

A

= ventricular fibrillation

357
Q

ALS: Management of ventricular fibrillation + pulseless ventricular tachycardia

A

= CPR + defibrillation

If persistent, Amiodarone 300mg IV (one-off dose) AND Adrenaline 1mg IV (can be given after the 3rd shock has been delivered)
(e.g., cycle 3, 5, 7 etc.)

[shockable rhythms]

358
Q

Investigation of choice in suspected spinal cord compression?

A

= urgent whole MRI

(aim to surgically decompress within 48 hours)

359
Q

Management for spinal cord compression (2)

A
  • urgent surgical decompression, typically within 24 hours
  • Dexamethasone (indicated in those with demonstrated malignancy on MRI, or those with high suspicion) - 16mg daily in divided doses - along with PPIs
360
Q

What is atrial fibrillation (AF)?

A

= characterised by irregular, uncoordinated atrial contraction usually at a rate of 300-600 beats per minute

361
Q

Commonest sustained cardiac arrhythmia?

A

= AF

362
Q

Definition of acute AF

A

= lasts < 48 hours

363
Q

Definition of paroxysmal AF

A

= lasts < 7 days, and is intermittent

364
Q

Definition of persistent AF

A

= lasts > 7 days but is amenable to cardioversion

365
Q

Definition of permanent AF?

A

= lasts > 7 days and is not amenable to cardioversion

366
Q

How do you define ‘fast’ vs ‘slow’ AF?

A

Fast AF: >/= 100 bpm
Slow AF: </= 60 bpm

367
Q

Most common cause of AF in the UK

A

= ischaemic heart disease

368
Q

Most common cause of AF in a less developed countries

A

= rheumatic heart disease

369
Q

Bedside test which can definitively diagnosis AF?

A

= 12-lead ECG

370
Q

ECG findings which suggest AF

A

= absence of p-waves, with irregularly irregular rhythm

371
Q

First-line treatment in a patient presenting with AF who is haemodynamically unstable

A

= synchronised DC cardioversion (+/- Amiodarone)

372
Q

Which of the following drugs can be used in AF rhythm control if patient has no structural heart disease?

  • Amiodarone
  • Flecainide
A
  • Flecainide
373
Q

Which of the following drugs can be used in AF rhythm control if patient has structural heart disease?

  • Amiodarone
  • Flecainide
A
  • Amiodarone
374
Q

Which of the following is the best option for stable patients presenting with AF - onset > 48 hours (or if onset unclear)?

  • rate + rhythm control
  • rate control only
  • rhythm control only
A
  • rate control only
375
Q

If patient presents with AF - onset > 48 hours, how long do they need to be anticoagulation for prior to attempting cardioversion?

A

= 3 weeks prior

(risk of throwing off a clot)

376
Q

How can you exclude a mural thrombus in patient with AF awaiting anticoagulation?

A

= TOE (transoesophageal echocardiogram)

377
Q

Is rate or rhythm control used first-line in most patients with AF?

A

= rate control

378
Q

1st line option for rate control in AF?

A

= beta-blocker (Bisoprolol) or, rate-limiting calcium channel blocker (Diltiazem)

379
Q

Final option for rhythm control in AF if cardioversion + pharmacological options don’t work?

A

= catheter ablation

380
Q

AF: What may be used for rate control in patients who have hypotension or have co-existing HF?

A

= Digoxin

381
Q

Why is Sotalol not used as a rate control agent in AF?

A

= because it also has rhythm control action

382
Q

AF: Which of the following rhythm control drugs are preferred in younger patients who have structurally normal hearts?

  • Flecainide
  • Amiodarone
  • Sotalol
A
  • Flecainide

(can induce fatal arrhythmias in those with structural heart disease)

383
Q

AF: Which of the following rhythm control drugs have a large number of significant SEs and so should only be given in older, sedentary patients?

  • Flecainide
  • Amiodarone
  • Sotalol
A
  • Amiodarone
384
Q

What can be used to stratify the risk of stroke in AF patients?

A

= CHADS2VASc Score

385
Q

CHADS2VASc Scoring System

A

C: congestive heart failure (1 point)
H: HTN (1 point)
A2: age >/= 75 (2 points)
D: DM (1 point)
S2: previous stroke or TIA (2 points)
V: vascular disease (1 point)
A: age 65-74 (1 point)
Sc: female (1 point)

386
Q

Score on CHADS2VASc which suggests patient should be anticoagulated?

(M + F)

A

Male: >/= 1
Female: >/= 2

387
Q

What is the ORBIT Score used for?

A

= used to assess risk of bleeding in patients with AF who are on anticoagulation

388
Q

First-line anticoagulation option in AF?

A

= DOACs

389
Q

Positives (2) and limitations (1) of using DOACs as anticoagulant in AF?

A

Positives:
- doesn’t require monitoring
- associated with fewer bleeding risks

Limitations:
- half-life approximately 12 hours, therefore if patient misses dose they are not covered

390
Q

Only oral anticoagulation licensed for valvular AF?

A

= Warfarin

391
Q

Why does initiating Warfarin require patient to have a cover with LMWH for 5 days?

A

= Warfarin is initially prothrombotic

392
Q

What is an acute thoracic dissection?

A

= occurs when a tear in the tunica intima of the aorta creates a false lumen whereby blood can flow between the inner and outer layers of the walls of the aorta

393
Q

Aortic Dissections: Standford Type A vs. Standford Type B

A

Stanford Type A: involves the ascending aorta, arch of the aorta

Stanford Type B: involves the descending aorta

394
Q

Imaging of choice to diagnose an aortic dissection?

A

= CT angiogram

395
Q

Management of aortic dissection (type A vs type B)

A

Type A: requires surgical management

Type B: normally managed conservatively with BP control
(if evidence of end organ damage than endovascular/ open repair may be performed

396
Q

Moderate asthma is characterised by which PEF range?

A

PEF > 50-70%

397
Q

Severe asthma is characterised by which PEF range?

A

= PEF 33-50%

398
Q

33,92 CHEST - mnemonic for features of life-threatening asthma

A

PEF < 33%
SO2 < 92%
Cyanosis
Hypotension
Exhaustion
Silent chest
Tachyarrhythmias

399
Q

What is ASA grading used for?

A

= allows anaesthetists to stratify the overall risk of a patient prior to surgery, and predicts short- and long-term outcomes

400
Q

ASA grade I

A

= normal healthy patients, who are non-smokers and with no/ minimal alcohol intake

401
Q

ASA grade II

A

= defined as patients with mild systemic disease e.g., well controlled diabetes, or hypertension, current smoker, obesity (BMI 30-40), and mild lung disease

402
Q

ASA grade III

A

= defined as patients with severe systemic disease e.g., poorly controlled diabetes or hypertension, COPD, morbid obesity (BMI >40), history of ACS/ stroke/ TIA < 3 months ago

403
Q

ASA guide IV

A

= defined as patients with severe systemic disease that is a constant threat to life e.g., MI/ stroke/ TIA within 3 months, severe valve dysfunction, severe reduction in ejection fraction, sepsis

404
Q

ASA grade V

A

= defined as moribund patients not expected to survive the operation e.g., ruptured abdominal aortic aneurysm, massive bleed, intracranial haemorrhage with mass effect

405
Q

ASA grade VI

A

= defined as a patient declared brain-dead whose organs are being removed for donation

406
Q

Simple airway manoeuvres (3)

A
  • suction
  • head tilt + chin lift
  • jaw thrust
407
Q

Which simple airway manoeuvre can be used when c-spine injury is suspected?

A

= jaw thrust

408
Q

Contraindication of using nasopharyngeal airway (NPA)?

A

= contraindicated in base of skill fracture

409
Q

What is NEXUS criteria used for?

A

= used to identify patients at low risk of C-spine injury. C-spine injury is unlikely if all of the criteria is met

410
Q

Imaging used in suspected c-spine injury

A

= CT c-spine

(plain x-rays are of limited value and not recommended)

411
Q
A

Year 4 (11 decks)

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