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1 - MSRA > Surgery > Flashcards

Surgery Flashcards

1
Q

Screening outcomes for abdominal aortic aneurysms

A

<3 cm - no further action
3 - 4.4cm - rescan every 12 months
4.5 - 5.4cm - rescan every 3 months
≥ 5.5cm - refer within 2 weeks to vascular surgery for probable intervention

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2
Q

Causes of acute pancreatitis

A
  • Gallstones
  • Ethanol
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune, Ascaris infection
  • Scorpion venom
  • Hypertriglyceridaemia, hyperchylomicronaemia, hypercalcaemia, hypothermia
  • ERCP
  • Drugs
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3
Q

Drugs causing acute pancreatitis

A
  • Azathioprine
  • Mesalazine
  • Didanosine
  • Bendroflumethiazide
  • Furosemide
  • Pentamidine
  • Steroids
  • Sodium valproate
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4
Q

Fasting before surgery

A
  • Clear fluids 2 hours
  • Non-clear fluids/foods 6 hours
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5
Q

Perioperative management of diabetics on insulin

A
  • If good glycaemic control and undergoing minor procedures, managed during op period with adjustment of usual income
  • If long fasting period of more than one issed meal, or poorly controlled diabetes, variable rate insulin infusion
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6
Q

Management of anti-diabetic drugs day prior to admission for elective surgery

A

Take as normal (unless OD insulin, then reduce dose by 20%)

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7
Q

Management of metformin on day of operation

A

If taken OD or BD - take as normal
If taken TDS - omit lunchtime dose

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8
Q

Management of sulfonylureas on day of operation (morning operation)

A

If taken OM - omit dose
If taken BD - omit morning dose

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9
Q

Management of sulfonylureas on day of operation (afternoon operation)

A

If taken OM - omit dose
If taken BD - omit both doses

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10
Q

Management of DPP IV inhibitors (-gliptins) on day of operation?

A

Take as normal

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11
Q

Management of GLP-1 inhibitors (-tides) on day of operation?

A

Take as normal

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12
Q

Management of SGLT-2 inhibitors (-flozins) on day of operation?

A

Omit on day of surgery

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13
Q

Management of OD insulin on day of operation?

A

Reduce dose by 20%

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14
Q

Management of twice daily biphasic or ultra-long acting insulins on day of operation

A

Halve usual morning dose, leave evening dose unchanged

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15
Q

Special preparation before thyroid surgery

A

Vocal cord surgery

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16
Q

Special preparation before parathyroid surgery

A

Consider methylene blue to identify gland

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17
Q

Special preparation before sentinel node biopsy

A

Radioactive marker/patent blue dye

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18
Q

Special preparation before surgery involving thoracic duct

A

Consider administration of cream

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19
Q

Special preparation before phaeochromocytoma surgery

A

Alpha and beta blockade

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20
Q

Special preparation before surgery for carcinoid tumour

A

Need covering with octreotide

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21
Q

Special preparation before colorectal cases

A

Bowel preperation

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22
Q

Special preparation before surgery for thyrotoxicosis

A

Lugols iodine/medical therapy

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23
Q

Features duodenal ulcer

A

Epigastric pain relieved by eating

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24
Q

Features gastric ulcer

A

Epigastric pain worsened by eating

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25
Q

Features appendicitis

A

Pain initially central abdomen before localising to right iliac fossa
Tachycardia
Low grade pyrexia
Tenderness in RIF

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26
Q

What is Rovsing’s sign, and when seen

A

More pain in RIF than LIF when palpating LIF
Seen in appendicits

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27
Q

Features acute pancreatitis

A

Severe epigastric pain
Vomiting

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28
Q

What is Cullen’s sign, when seen

A

Periumbilical discolouration
Acute pancreatitis

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29
Q

What is Grey-Turner’s sign, when seen

A

Flank discolouration
Acute pancreatitis

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30
Q

Features biliary colic

A

Pain in RUQ radiating to back and interscapular region
May follow fatty meal

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31
Q

Acute cholecystitis features

A

History of gallstones symptoms
Continuous RUQ pain
Fever

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32
Q

Murphys sign and when seen

A

Arrest of inspiration on palpation of RUQ
Acute cholecystitis

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33
Q

Diverticulitis features

A

Colicky pain, typically LLQ
Fever

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34
Q

Abdominal aortic aneurysm features

A

Severe central abdominal pain radiating to back
Presentation may be catastrophic (sudden collapse) or subacute (persistent severe abdominal pain with developing shock)

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35
Q

Intestinal obstruction features

A

Vomiting
BNO
Tinkling BS

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36
Q

Location inguinal hernia

A

Above and medial to pubic tubercle

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37
Q

Location femoral hernia

A

Below and lateral pubic tubercle

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38
Q

Demographic inguinal hernia

A

95% male

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39
Q

Risk of strangulation inguinal hernia

A

Rare

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40
Q

Demographic femoral hernia

A

More common in women, particularly multiparous

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41
Q

Risk of strangulation femoral hernia

A

High

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42
Q

Features umbilical hernia

A

Symmetrical bulge under umbilicus

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43
Q

Features paraumbilical hernia

A

Asymmetrical bulge, half sac covered by skin of abdomen directly above or below the umbilicus

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44
Q

Features epigastric hernia

A

Lump in midline between umbilicus and xiphisternum

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45
Q

What is spigelian hernia

A

Hernia through spigelian fascia, which is aponeurotic layer between rectus abdominis muscle medially and semilunar line laterally

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46
Q

What is obturator hernia

A

Hernia passes through obturator foramen (medial thigh)

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47
Q

Demographic obturator hernia

A

More common in women

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48
Q

Presentation obturator hernia

A

Typically presents with bowel obstruction

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49
Q

What is Richter hernia

A

Rare
Only antimesenteric border of bowel herniates through fascial defect

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50
Q

Presentation Richter hernia

A

Strangulation without symptoms of obstruction

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51
Q

Mechanism congenital inguinal hernia

A

Indirect hernia resulting from patent processus vaginalis

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52
Q

Management congenital inguinal hernia

A

Surgically repaired soon after diagnosis as risk of incarceration

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53
Q

Risk factors infantile umbilical hernia

A

Premature
Afro-Caribbean

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54
Q

Management infantile umbilical hernia

A

Monitor - vast majority resolve without intervention before 4-5 years, complications are rare

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55
Q

Risk factors abdominal wound dehiscence

A

Malnutrition
Vitamin deficiencies
Jaundice
Steroid use
Major wound contamination, e.g. faecal peritonitis
Poor surgical technique

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56
Q

Treatment abdominal wound dehiscence

A

Coverage of wound with saline impregnated gauze
IV broad spectrum antibiotics
Analgesia
IV fluids
Return to theatre

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57
Q

Psoas sign and where seen

A

Pain on extending hip
Retrocaecal appendicitis

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58
Q

Blood findings appendicitis

A

Raised inflammatory markers
Neutrophil-predominant leucocytosis

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59
Q

Role of urinalysis in appendicitis

A

Exclude pregnancy, renal colic, and UTI
In appendicitis, may show mild leucocytosis but no nitrates

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60
Q

Management appendicitis

A

Appendicectomy with prophylactic IV antibiotics

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61
Q

Purpose of IV antibiotics in appendicectomy

A

Reduce wound infection rates

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62
Q

What is required in perforated appendicitis

A

Copious abdominal lavage

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63
Q

Complications acute pancreatitis

A

Peripancreatic fluid collections
Pseudocysts
Pancreatic necrosis
Pancreatic abscess
Haemorrhage
ARDS

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64
Q

Incidence peripancreatic fluid collection

A

25%

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65
Q

Features peripancreatic fluid collections

A

Located in or near pancreas
Lack wall of granulation or fibrous tissue
May resolve or develop into pseudocysts or abscesses

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66
Q

Management peripancreatic fluid collection

A

Since may resolve, avoid aspiration and drainage - may precipitate infection

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67
Q

How do pancreatic pseudocysts develop after acute pancreatitis

A

Result from organisation of peripancreatic fluid collection, may or may not communicate with ductal system.

Collection walled by fibrous or granulation tissue

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68
Q

When do pseudocysts occur after acute pancreatitis

A

Typically 4+ weeks

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69
Q

Bloods pancreatic pseudocyst

A

75% mild elevation of amylase

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70
Q

Investigations pancreatic pseudocyst

A

CT
ERCP
MRI
Endoscopic USS

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71
Q

Management pancreatic pseudocysts

A

Observation up to 12 weeks - up to 50% resolve
Treatment with endoscopic or surgical cystogastrostomy or aspiration

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72
Q

Location pancreatic necrosis complicating acute pancreatitis

A

May involve pancreatic parenchyma and surrounding fat

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73
Q

Management pancreatic necrosis

A

Sterile necrosis managed conservatively
Early necrosectomy high mortality, should be avoided if possible

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74
Q

What is pancreatic abscess

A

Intra-abdominal collection of pus associated with pancreas, but absence of necrosis
Typically result from infected pseudocyst

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75
Q

Management pancreatic abscess

A

Transgastric drainage or endoscopic drainage

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76
Q

What causes haemorrhage post-pancreatitis

A

Infected necrosis may involve vascular structures with resultant haemorrhage, may occur de novo or result of surgical necrosectomy

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77
Q

Acute pancreatitis management

A

Fluid resuscitation
Analgesia
Nutrition

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78
Q

Fluid resuscitation in acute pancreatitis

A

Aggressive early hydration with crystalloids, aim UO >0.5ml/kg/hour

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79
Q

Analgesia in acute pancreatitis

A

IV opioids usually required

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80
Q

Nutrition acute pancreatiits

A

Not routinely NBM unless clear reason
Enteral nutrition offered to anyone with moderate severe or severe acute pancreatitis within 72h of presentation

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81
Q

Role of parenteral nutrition in acute pancreatitis

A

Should only be used if enteral nutrition failed or contraindicated

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82
Q

Role of antibiotics in acute pancreatitis

A

Prophylactic antibiotics not routinely offered
Used in infected pancreatic necrosis

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83
Q

Criteria mild acute pancreatitis

A

No organ failure, no local complications

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84
Q

Criteria moderately severe acute pancreatitits

A

No or transient organ failure (<48 hours), possible local complications

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85
Q

Criteria severe acute pancreatitis

A

Persistent organ failure, possible local complications

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86
Q

Indications for surgery acute pancreatitis

A
  • Gallstones
  • Obstructed biliary system due to stones
  • Fail to settle with necrosis and worsening organ dysfunction
  • Infected necrosis
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87
Q

Management acute pancreatitis caused by gallstones

A

Early cholecystectomy

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88
Q

Management acute pancreatitis with obstructed biliary system due to stones

A

Early ERCP

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89
Q

Management acute pancreatitis with necrosis and worsening organ dysfunction

A

Debridement or fine needle aspiration

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90
Q

Management acute pancreatitis with infected necrosis

A

Radiological drainage or surgical necrosectomy

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91
Q

ASA 1

A

Normal healthy patient

Non-smoker, no or minimal alcohol use

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92
Q

ASA 2

A

Patient with mild systemic disease without substantiative functional limitations

E.g. smoker, social alcohol drinker, pregnancy, obesity, well controlled diabetes/hypertension

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93
Q

ASA 3

A

Patient with severe systemic disease

Substantiative functional limitations, one or more moderate to severe diseases

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94
Q

ASA 4

A

Severe systemic disease that is constant threat to life

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95
Q

ASA 5

A

Moribund patient not expected to survive without the operation

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96
Q

ASA 6

A

Declared brain-dead patient for organ retrieval

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97
Q

Management acute anal fissure

A

Soften stool - dietary advice, bulk-forming laxatives, if not tolerated then lactulose
Lubricants, e.g. petroleum jelly
Topical anaesthetic

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98
Q

Management chronic anal fissure

A

Acute treatments continued
Topical GTN
If not effective after 8 weeks, referral for sphincterotomy or botulinum toxin

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99
Q
A
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100
Q

Location of anal fissure

A

90% posterior midline (if other location, consider underlying cause e.g. Crohn’s)

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101
Q

Most common organisms anorectal abscess

A

E. coli
Staph aureus

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102
Q

Causes rectal prolapse

A

Childbirth
Rectal intussusception

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103
Q

Causes solitary rectal ulcer

A

Chronic staining and constipation

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104
Q

Histology solitary rectal ulcer

A

Mucosal thickening
Lamina propria replaced with collagen and smooth muscle

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105
Q

Types of anti-oestrogen drugs

A

SERM (selective oestrogen receptor modulators)
Aromatase inhibitors

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106
Q

Example SERM

A

Tamoxifen

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107
Q

Role of tamoxifen

A

Oestrogen receptor positive breast cancer treatment

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108
Q

Adverse effects tamoxigen

A

Menstrual disturbance - vaginal bleeding, amenorrhoea
Hot flushes
VTE
Endometrial cancer

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109
Q

Examples aromatase inhibitors

A

Anastrozole
Letrozole

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110
Q

Mechanism of action aromatase inhibitors

A

Reduce peripheral oestrogen synthesis

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111
Q

Role aromatase inhibitors

A

Treatment of oestrogen receptor +ve breast cancer in post-menopausal women

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112
Q

Adverse effects aromatase inhibitors

A

Osteoporosis
Hot flushes
Arthralgia, myalgia
Insomnia

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113
Q

Most common organism ascending cholangitis

A

E coli

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114
Q

Features ascending cholangitis

A

RUQ pain
Fever
Jaundice
(Charcots triad)

Hypotension
Confusion
(Reynolds’ pentad)

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115
Q

First line investigation ascending cholangitis

A

Ultrasound - bile duct dilatation and stones

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116
Q

Management ascending cholangitis

A

IV antibiotics
ERCP after 24-48 hours

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117
Q

Features fibroadenoma

A

Mobile, firm breast lump

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118
Q

Risk of malignancy fibroadenoma

A

No increased risk of malignancy

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119
Q

Treatment fibroadenoma

A

Surgical excision if >3cm

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120
Q

Features breast cyst

A

Smooth discrete lump, may be fluctuant

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121
Q

Risk of malignancy breast cyst

A

Small increased risk of breast cancer, especially if younger

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122
Q

Management breast cyst

A

Cysts should be aspirated

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123
Q

When does breast cyst need biopsy/excision

A

If aspirate blood stained or persistently refill

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124
Q

Sclerosing adenosis presentation

A

Breast lump or breast pain
Mammographic changes - may mimic carcinoma

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125
Q

Sclerosing adenosis malignancy risk

A

No increase in malignancy risk

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126
Q

Treatment sclerosing adenosis

A

Lesions should be biopsied, excision not mandatory

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127
Q

Epithelial hyperplasia presentation

A

Variable, from generalised lumpiness to discrete lump

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128
Q

Epithelial hyperplasia malignancy risk

A

Increased risk of malignancy, particularly if atypical features or family history

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129
Q

Treatment epithelial hyperplasia

A

If no atypical features, conservative management
If atypical features, either close monitoring or surgical resection

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130
Q

Causes fat necrosis

A

40% cases traumatic aetiology

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131
Q

Management fat necrosis

A

Imaging and core biopsy

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132
Q

Presentation duct papilloma

A

Usually present with nipple discharge
Large papillomas may present with mass

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133
Q

Duct papilloma risk of malignancy

A

No increased risk of malignancy

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134
Q

Management duct papilloma

A

Microdochectomy

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135
Q

First line treatment BPH

A

Alpha 1 antagonists, e.g. tamsulosin, alfuzosin

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136
Q

Mechanism of action alpha 1 antagonists in BPH

A

Decrease smooth muscle tone of prostate and bladder

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137
Q

Adverse effects alpha 1 antagonists

A

Dizziness
Postural hypotension
Dry mouth
Depression

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138
Q

Other treatment options BPH

A

5 alpha reductase inhibitors e.g. finasteride
Antimuscarinics
Surgery

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139
Q

Role of finasteride BPH

A

Indicated if significantly enlarged prostate and high risk of progression

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140
Q

Advantage of finasteride over tamsulosin

A

Cause reduction in prostate volume, so may slow progression

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141
Q

Limitation of finasteride BPH

A

Symptoms don’t improve for 6 months

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142
Q

Adverse effects finasteride

A

Erectile dysfunction
Reduced libido
Ejaculation problems
Gynaecomastia

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143
Q

Role of antimuscarinics BPH

A

If mixture of storage symptoms and voiding symptoms persisting after treatment with alpha blocker alone

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144
Q

Examples antimuscarinic used in BPH

A

Tolterodine
Darifenacin

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145
Q

Drugs causing gallstones

A

Fibrates
COCP

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146
Q

Features biliary colic

A

Right upper abdominal pain, worse after eating and after fatty foods, may radiate to right shoulder/interscapular region
Nausea and vomiting common

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147
Q

Management biliary colic

A

Elective laparoscopic cholecystectomy

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148
Q

AXR duodenal atresia

A

Double bubble sign

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149
Q

Investigation findings malrotation with volvulus

A

Upper GI contrast - DJ flexure more medially placed
USS - abnormal orientiation of SMA and SMV

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150
Q

Treatment malrotation with volvulus

A

Ladd’s procedure

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151
Q

AXR jejunal/ileal atresia

A

Air-fluid levels

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152
Q

Treatment jejunal/ileal atresia

A

Laparotomy with primary resection and anastomosis

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153
Q

AXR findings mec ileus

A

Air fluid level

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154
Q

Treatment mec ileus

A

Surgical decompression
Serosal damage may need segmental resection

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155
Q

Incidence mec ileus in cystic fibrosis

A

15-20%

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156
Q

AXR NEC

A

Dilated bowel loops
Pneumatosis
Portal venous air

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157
Q

Treatment NEC

A

Conservative and supportive if non-perf
Laparotomy and resection in perforation or ongoing deterioration

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158
Q

RF transitional cell bladder cancer

A

Smoking - most important in Western countries
Aniline dyes, e.g. printing and textile industry workers
Rubber manufacture
Cyclophosphamide

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159
Q

RF squamous cell bladder cancer

A

Schistosomiasis
Smoking

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160
Q

Criteria for brain stem death testing

A
  • Deep coma of known aetiology
  • Reversible causes excluded
  • No sedation
  • Normal electrolytes
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161
Q

Testing for brain death

A

Fixed pupils, dont respond to light
No corneal reflex
Absent oculo-vesticular reflexes
No response to supraorbital pressure
No cough reflex to bronchial stimulation, or gagging response to pharyngeal stimulation
No observed respiratory effort in response to disconnection of ventilator

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162
Q

How are oculo-vesticular reflexes tested in brain death

A

No eye movements following the slow injection of at least 50ml of ice-cold water into each ear in turn

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163
Q

Requirements for doctors performing brain stem death testing

A

Two doctors on two occasions
Both experienced in brain stem death testing
At least 5 years post-grad experience
One must be a consultant
Neither can be member of transplant team

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164
Q

Most common organism causing breast abscess in lactational women

A

Staphylococcus aureus

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165
Q

Presentation breast abscess

A

Tender, fluctuant mass in lactating women

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166
Q

Management breast abscess

A

I&D or needle aspiration
Antibiotics should be given

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167
Q

Determination of surgical management in breast cancer with no palpable lymphadenopathy

A

Should have pre-op axillary ultrasound before their primary surgery. If negative, should have sentinal node biopsy to assess nodal burden

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168
Q

Surgical management breast cancer with palpable lymphadenopathy

A

Axillary node clearance at primary surgery

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169
Q

SEs axillary node clearance in breast cancer

A

Arm lymphodema and functional arm impairment

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170
Q

Indications for mastectomy breast cancer

A

Multifocal tumour
Central tumour
Large lesion in small breast
DCIS >4cm

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171
Q

Indications for wide local excision breast cancer

A

Solitary lesion
Peripheral tumour
Small lesion in large breast
DCIS <4cm

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172
Q

Who is offered radiotherapy breast cancer

A

All wide local excision
If mastectomy, T3-4 tumours and 4+ positive axillary nodes

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173
Q

Who is offered hormonal therapy breast cancer

A

Hormone receptor positive tumours

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174
Q

Hormone therapy breast cancer

A

Tamoxifen in pre- and peri-menopausal women
Aromatase inhibitors e.g. anastrozole in post-menopausal women

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175
Q

Why are aromatase inhibitors offered to post-menopausal women with ER+ve breast cancer

A

Aromatisation accounts for majority of oestrogen production in this group

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176
Q

SE’s tamoxifen

A

Increased risk of endometrial cancer
Increased risk VTE
Menopausal symptoms

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177
Q

Most common type of biological therapy breast cancer

A

Trastuzumab (herceptin)

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178
Q

Who is offered herceptin

A

HER2 positive (only useful in 20-25%)

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179
Q

Herceptin contraindication

A

History of heart disorders

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180
Q

2WW breast cancer referral criteria

A
  • 30+ unexplained breast lump
  • 50+ unilateral nipple discharge, retraction, or other changes of concern
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181
Q

Criteria consider 2WW referral breast cancer

A

Skin changes suggesting breast cancer
30+ unexplained lump in axilla

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182
Q

Non-urgent breast referral criteria

A

Under 30 with unexplained breast lump with or without pain

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183
Q

Breast cancer risk factors

A

BRCA1/2 mutation
Nulliparity, first pregnancy >30 years
Early menarche, late menopause
COCP, combined HRT
Past breast cancer
Not breastfeeding
Ionising radiation
p53 mutation
Obesity
Previous surgery for benign breast disease

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184
Q

NHS breast cancer screening programme schedule

A

Mammogram 3 yearly in 50-70y/o

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185
Q

Who needs referring for familial breast cancer

A

If one first or second degree relative with breast cancer and:
Age of diagnosis <40 years
Bilateral breast cancer
Male breast cancer
Ovarian cancer
Jewish ancestry
Sarcoma in relative younger than age 45 years
Glioma or childhood adrenal cortical carcinomas
Complicated patterns of multiple cancers at young age
Paternal history of breast cancer (2+ relatives on fathers side)

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186
Q

Which patients should be referred for early screening due to family history of breast cancer

A
  • 1st relative diagnosed with breast cancer younger than 40
  • 1st degree male related diagnosed with breast cancer
  • 1st degree relative with bilateral breast cancer (if 1st primary diagnosed younger than 50)
  • 2 1st relatives, or 1 1st + 1 2nd
  • 1 1/2nd relative breast cancer + 1 1/2nd relative ovarian cancer
  • 3 2nd degree breast cancer any age
187
Q

Most common types of breast cancer

A

Invasive ductal carcinoma (most common)
Invasive lobular carcinoma
Ductal carcinoma in situ
Lobular carcinoma in situ

188
Q

Invasive carcinoma vs carcinoma in situ (breast)

A

Carcinoma in situ has not spread beyond local tissue, invasive carcinoma has

189
Q

What is Paget’s disease of nipple

A

Eczematous change of nipple associated with underlying breast malignancy

190
Q

Cause inflammatory breast cancer

A

Cancerous cells block lymph drainage resulting in inflamed appearance of breast

191
Q

Features fibroadenoma

A

Discrete, non-tender, highly mobile breast lumps - ‘breast mice’

192
Q

Fibroadenoma demographic

A

Common in women under 30

193
Q

Features fibroadenosis

A

Lumpy breasts
May be painful
Symptoms may worsen prior to menstruation

194
Q

Demographic fibroadenosis

A

Middle aged women

195
Q

Features mammary duct ectasia

A

Tender lump around areola
May be green nipple discharge
If ruptures, may cause local inflammation - ‘plasma cell mastitis’

196
Q

Demographic mammary duct ectasia

A

Most common around menopause

197
Q

What is duct papilloma

A

Local areas of epithelial proliferation in large mammary ducts

198
Q

Presentation duct papilloma

A

Blood stained discharge

199
Q

Is duct papilloma malignant?

A

No - hyperplastic lesions rather than malignant/premalignant

200
Q

Demographic fat necrosis

A

Obese women with large breasts

201
Q

Features fat necrosis

A

Initial inflammatory response
Lesion firm and round, may develop into hard, irregular breast lump
May mimic breast cancer, so further investigation always warranted

202
Q

Causes chronic pancreatitis

A

Alcohol excess - 80% of cases
Cystic fibrosis
Haemochromatosis
Ductal obstruction - tumours, stones, structural abnormalities

203
Q

Features chronic pancreatitis

A

Pain worse 15-30 mins after meal
Steatorrhoea (5-25 years after onset of pain)
Diabetes mellitus (20 years after onset of pain

204
Q

Abdominal XR chronic pancreatitis

A

Pancreatic calcification in 30% of cases

205
Q

Abdominal XR vs CT in chronic pancreatitis

A

CT more sensitive at detecting pancreatic calcification - 80%

206
Q

Functional tests chronic pancreatitis

A

Faecal elastase - used if imaging inconclusive

207
Q

Management chronic pancreatitis

A

Pancreatic enzyme supplements
Analgesia
Antioxidants

208
Q

Staging investigations newly diagnosed colorectal cancer

A

CEA
CT CAP
Entire colon colonoscopy or CT colonography
If tumour below peritoneal reflection, MRI of mesorectum

209
Q

Surgical options colonic cancer presenting with obstruction

A

Stent or resection

210
Q

Indications right hemicolectomy colon cancer

A

Caecal, ascending, or proximal transverse colon tumour

211
Q

Indications for left hemicolectomy colon cancer

A

Distal transverse or descending colon tumour

212
Q

Indications for high anterior resection colon cancer

A

Sigmoid colon tumour

213
Q

Indications for anterior resection colon cancer

A

Rectal tumour

214
Q

Indications for abdomino-perineal excision colon cancer

A

Anal verge tumour

215
Q

Role of chemo colon cancer

A

Used in neoadjuvant setting (particularly rectal cancer), adjuvant setting, and metastatic disease

216
Q

Role of radiotherapy colon cancer

A

Predominantly rectal cancers in neoadjuvant or adjuvant setting

217
Q

Targeted therapies used in colon cancer

A

Bevacizumab
Cetuximab

Particularly used in metastatic disease

218
Q

What is Hartmann’s procedure

A

Resection of sigmoid colon and end colostomy fashioned

219
Q

When should FIT test guide referral colorectal cancer

A
  • Abdominal mass
  • Change in bowel habit
  • Iron deficiency anaemia
  • Age 40+ with unexplained weight loss and abdo pain
  • Age under 50 with rectal bleeding and abdominal pain or weight loss
  • Age 50+ with unexplained rectal bleeding, abdominal pain, or weight loss
  • Age 60+ with anaemia
220
Q

Who does not need FIT test before 2WW colorectal cancer referral

A

Rectal mass
Unexplained anal mass
Unexplained anal ulceration

221
Q

What to do if negative FIT test (done for symptoms)

A

Safety netting
Referring on suspected cancer pathway if ongoing significant concern, e.g. abdo mass

222
Q

Colorectal cancer screening programme - who and when

A

All men and women 60-74 years (50-74 in Scotland), ever 2 years

223
Q

What to do with abnormal FIT results (screening)

A

Offer colonoscopy

224
Q

When is FIT test recommended (not meeting 2WW criteria)

A

≥ 50 with unexplained abdominal pain or weight loss
< 60 with changes in bowel habit or iron deficiency anaemia
≥ 60 with anaemia

225
Q

ECG findings hyperkalaemia

A

Peaked or ‘tall tented’ T waves
Loss of P wabes
Broad QRS complexes
Sinusoidal wave pattern
Ventricular fibrillation

226
Q

Features epididymal cysts

A

Seperate from body of testicle
Found posterior to testicle

227
Q

Conditions associated with epididymal cysts

A
  • PKD
  • Cystic fibrosis
  • Von-Hippel-Lindau syndrome
228
Q

Most common organism causing epididymo-orchitis

A

Chlamydia trachomatis and Neisseria gonorrhoae in sexually active younger adults
E. coli in older adults

229
Q

Features epididymo-orchitis

A

Unilateral testicular pain and swelling

230
Q

Management epididymo-orchtis

A

If STI most likely, refer GUM. If unknown organism, ceftriaxone IM + doxycycline PO
If enteric organisms most likely, send MSU and oral quinolone

231
Q

Features femoral hernia

A

Lump within groin, mildly painful
Inferolateral to pubic tubercle
Normally non-reducible
Cough impulse often absent (due to small size of femoral ring)

232
Q

Epidemiology femoral hernias

A

Less common than inguinal - 5% of abdominal hernias
More common in women, more common in multiparous

233
Q

Investigation femoral hernia

A

Diagnosis usually clinical, ultrasound if doubt

234
Q

Complications femoral hernia

A

Incarceration
Strangulation
Bowel obstruction → ischaemia

235
Q

Presentation femoral hernia strangulation

A

Lump tender and non-reducible
Systemically unwell patient

236
Q

Management femoral hernias

A

Surgical repair necessary - laparoscopic or laparotomy

237
Q

Indication for fluid resuscitation in burns

A

> 15% TBSA burns (10% in children)

238
Q

Why is fluid resuscitation needed in burns

A

Most fluid is lost 24 hours after the injury
In first 8-12 hours, fluid shifts from intravascular to interstitial fluid compartments, so circulatory volume compromised

239
Q

Calculation for fluid resuscitation in burns

A

Total fluid requirement in 24 hours = 4ml x TBSA % x weight (kg)

Deduct fluids already given

240
Q

Over what time period is fluid resuscitation given in burns

A

50% in first 8 hours
50% in next 16 hours

Starting point time of injury

241
Q

What is the goal of fluid resuscitation in burns?

A

UO 0.5 - 1.0 ml/kg/hour

242
Q

How should fluids be managed after the initial 24 hours in burns

A

Colloid infusion at rate of 0.5ml x TBSA x weight
Maintenance crystalloid (usually dex/saline) continued at rate of 1.5ml x TBSA x weight

243
Q

What kind of burns might require more fluids

A

High tension electrical injuries and inhalation injuries

244
Q

What should be monitored in burns

A
  • Packed cell volume
  • Plasma sodium
  • Base excess
  • Lactate
245
Q

Examples volatile liquid anaesthestics

A

Isoflurane
Desflurane
Sevoflurane

246
Q

Adverse effects volatile liquid anaesthetics

A

Myocardial depression
Malignant hyperthermia

247
Q

Adverse effects nitrous oxide

A

May diffuse into gas filled compartments → increase in pressure, so avoid in certain conditions e.g. pneumothorax

248
Q

Adverse effects propofol

A

Pain on injection
Hypotension

249
Q

Adverse effects thiopental

A

Laryngospasm

250
Q

Adverse effects etomidate

A

Primary adrenal suppression
Myoclonus

251
Q

Adverse effects ketamine

A

Disorientation
Hallucinations

252
Q

Use volatile liquid anaesthetics

A

Induction and maint anaesthesia

253
Q

Use nitrous oxide

A

Maintenance anaesthesia
Analgesia, e.g. during labour

254
Q

Use propofol

A

Induction general anaesthesia
In ICU for ventilated patients
Some anti-emetic properties (useful if high risk of PONV)

255
Q

Properties of thiopental

A

Highly lipid soluble, so quickly affects brain

256
Q

Features etomidate

A

Causes less hypotension than propofol and thiopental during induction, therefore used in cases of haemodynamic instability

257
Q

Features ketamine

A

Acts as dissociative anaesthetic
Doesn’t cause drop in BP, so useful in trauma

258
Q

Features haemorrhoids

A

Painless rectal bleeding (most common)
Pruritis
Pain - usually not significant unless thrombosed
Soiling (3rd/4th degree)

259
Q

Internal vs external haemorrhage

A

External originate below dentate line, prone to thrombosis and may be painful
Internal originate above dentate line, do not generally cause pain

260
Q

Grade I internal haemorrhoids definition

A

Do not prolapse out of the anal canal

261
Q

Grade II internal haemorrhoids definition

A

Prolapse on defecation, but reduce spontaneously

262
Q

Grade III internal haemorrhoids definition

A

Can be manually reduced

263
Q

Grade IV internal haemorrhoids definition

A

Cannot be reduced

264
Q

Primary care management haemorrhoids

A

Soften stools - increase dietary fibre and fluid intake
Topical local anaesthetic
Topical steroids

265
Q

Outpatient surgical management haemorrhoids

A

Rubber band ligation
Injection sclerotherapy

266
Q

When is surgery used in haemorrhoids

A

Large symptomatic haemorrhoids which do not respond to outpatient treatments

267
Q

Presentation acutely thrombosed external haemorrhoids

A

Significant pain
Purplish, oedematous, tender subcutaneous perianal mass

268
Q

Management acutely thrombosed external haemorrhoids

A

If present within 72 hours, referral for excision
Otherwise, manage with stool softeners, ice packs, analgesia

269
Q

Where is bleeding extradural haemorrhage

A

Between dura mater and skull

Most occur in temporal region as skull fracture cause a rupture of middle meningeal artery

270
Q

Causes extradural haemorrhage

A

Acceleration-deceleration trauma
Blow side of head

271
Q

Features extradural haemorrhage

A

Raised ICP
Some patients may have lucid interval

272
Q

Where is bleeding subdural haematoma

A

Outermost meningeal layer

Most around frontal and parietal lobes

273
Q

Risk factors subdural haematoma

A

Old age
Alcoholism

274
Q

Cause diffuse axonal injury

A

Mechanical shearing following deceleration, causing disruption and tearing of axons

275
Q

What causes secondary brain injury

A

When cerebral oedema, ischaemia, infection, tonsillar or tentorial herniation exacerbates the original injury.
Normal cerebal autoregulatory processes are disrupted following trauma, rendering brain more susceptible to blood flow changes and hypoxia

276
Q

Management life threatening ICP rise whilst theatre/transfer sorted

A

IV mannitol/furosemide

277
Q

Management diffuse cerebral oedema

A

May require decompressive craniotomy

278
Q

Management skull fractures

A

Depressed skull fractures that are open require formal surgical reduction and debridement
Closed injuries can be managed non-operatively if minimal displacement

279
Q

When is ICP monitoring used in head injury

A

Appropriate if GCS 3-8 and normal CT scan
Mandatory if GCS 3-8 and abnormal CT scan

280
Q

Cause of hyponatraemia in head injury

A

Most likely SIADH

281
Q

Minimum cerebral perfusion pressure in adults

A

70mmHg

282
Q

Minimum cerebral perfusion pressure in children

A

40-70mmHg

283
Q

Cause of unilaterally dilated, sluggish/fixed pupil in head injury

A

3rd nerve compression secondary to tentorial herniation

284
Q

Cause of bilaterally dilated, sluggish/fixed pupil in head injury

A

Poor CNS perfusion
Bilateral 3rd nerve palsy

285
Q

Cause of pupils cross reactive to light

A

Optic nerve injury

286
Q

Cause of bilaterally constricted pupils

A

Opiates
Pontine lesions
Metabolic encephalopathy

287
Q

Cause of unilaterally constricted pupils

A

Sympathetic pathway disruption

288
Q

Criteria for CT head within 1 hour

A

GCS <13 on initial assessment
GCS <15 2 hours post injury
Suspected open or depressed skull fracture
Any sign of basal skull fracture
Post-traumatic seizure
Focal neurological deficit
More than 1 episode of vomiting

289
Q

Criteria for CT head within 8 hours of injury

A

Adults with any of following that have had some loss of consciousness or amnesia since injury:
- Age 65 or older
- Any history of bleeding or clotting disorders including anticoagulants
- Dangerous mechanism of injury (fall over 1m/5 stairs)
- More than 30 mins retrograde amnesia of events immediately before head injury

If patient on warfarin

290
Q

What is a hiatus hernia

A

Herniation of part of stomach above the diaphragm

291
Q

Types of hiatus hernia

A

Sliding (95%) - GI junction moves above the diaphragm
Rolling - GI junction remains below, but seperate part of stomach herniates through oesophageal hiatus

292
Q

Features hiatus hernia

A

Heartburn
Dysphagia
Regurgitation
Chest pain

293
Q

Investigation hiatus hernia

A

Barium swallow - most sensitive

294
Q

Management hiatus hernia

A

Conservative management - weight loss
Medical management - PPI

Surgical management only in symptomatic rolling hernia

295
Q

Cause hydatid cysts

A

Tapeworm parasite Echinococcus granulosus

296
Q

Pathophysiology hydatid cysts

A

Outer fibrous capsule formed containing multiple smaller daughter cysts. These cysts are allergens causing type 1 hypersensitivity reaction

297
Q

Location hydatid cysts

A

90% in liver and lungs

298
Q

Cause of morbidity hydatid cysts

A
  • Cyst bursting
  • Infection
  • Organ dysfunction - biliary, bronchial, renal, and CSF outflow obstruction
299
Q

Investigation hydatid cysts

A

Ultrasound first line
CT best to differentiate from amoebic and pyogenic cysts
Serology

300
Q

Treatment hydatid cysts

A

Surgery

301
Q

Consideration surgery for hydatid cysts

A

Cyst walls must not be ruptured during removal, and contents sterilised first

302
Q

What is hydrocele

A

Accumulation of fluid in tunica vaginalis

303
Q

Types of hydrocele

A

Communicating
Non-communicating

304
Q

Cause communicating hydrocele

A

Patency of processus vaginalis allowing peritoneal fluid to drain into scrotum

305
Q

Who gets communicating hydroceles

A

Newborns

306
Q

Outcome communicating hydroceles

A

Usually resolve in first few months of life

307
Q

Cause non-communicating hydroceles

A

Excessive fluid production within tunica vaginalis

May develop secondary to epididymo-orchitis, testicular torsion, testicular tumours

308
Q

Features hydrocele

A

Soft, non-tender swelling of hemiscrotum
Usually anterior to and below testicle
Swelling confined to scrotum - can get above mass
Transilluminates

309
Q

Diagnosis hydrocele

A

Clinical, but USS required if any doubt about diagnosis, or underlying testis can’t be palpated

310
Q

Management hydrocele

A

Usually conservative approach

311
Q

Presentation inguinal hernias

A

95% men
Groin lump superior and medial to pubic tubercle, disappears on pressure/lying down
Discomfort and ache, often worse with activity, severe pain uncommon

312
Q

Management inguinal hernia

A

Treat even if asyptomatic - mesh repair. Unilateral open, bilateral/recurrent laparoscopic

313
Q

Time off work inguinal hernia

A

Return to non-manual work after 2-3 weeks in open repair, 1-2 laparoscopic

314
Q

Causes lidocaine toxicity

A

IV or excess administrationRi

315
Q

Risk factors lidocaine toxicity

A

Liver dysfunction
Low protein states

316
Q

Treatment local anaesthetic toxicity

A

IV 20% lipid emulsion

317
Q

Drug interactions lidocaine

A

Beta blockers
Ciprofloxacin
Phenytoin

318
Q

Features of lidocaine toxicity

A

Initially CNS over-activity then depression
Cardiac arrhythmiasa

319
Q

Use of cocaine hydrochloride

A

Limited use in ENT surgery - applied topically to nasal mucosa, rapid onset of action and causes marked vasoconstriction

320
Q

Use of bupivacaine

A

Wound infiltration at conclusion of surgical procedures for long duration analgesic effect

321
Q

Limitation of bupivacaine

A

Cardiotoxic, so contraindicated in regional blockage in case tourniquet fails

322
Q

Bupivacaine vs levobupivicaine

A

Levobupivicaine is less cardiotoxic and causes less vasodilation

323
Q

Use of prilocaine

A

Agent of choice in IV regional anaesthesia (less cardiotoxic than other ages)

324
Q

Affect of adrenaline with local anaesthetic

A

Can be added to local anaesthetic, prolongs duration of action at site of injection and permits high doses

325
Q

Contraindications adrenaline use with local anaesthetic

A

MAOI or TCA use

326
Q

Options for management of predominantly voiding LUTS in men

A
  • Conservative management
  • Alpha blocker
  • 5 alpha reductaes inhibitor
  • Antimuscarinic
327
Q

Conservative measures voiding LUTS in men

A
  • Pelvic floor muscle training
  • Bladder training
  • Prudent fluid intake
  • Containment products
328
Q

When to offer alpha blocker voiding LUTS men

A

Moderate or severe symptoms

329
Q

When to offer 5-alpha reductase inhibitor voiding LUTS men

A

If prostate is enlarged and patient considered high rik of progression

330
Q

How to manage voiding LUTS when prostate enlarged and moderate/severe symptoms

A

Both alpha blocker and 5 alpha reductase inhibitor

331
Q

When should antimuscarinic be offered voiding LUTS men

A

If mixed symptoms of voiding and storage not responding to alpha blocker

332
Q

First line treatment predominantly overactive bladder symptoms men

A

Conservative measures - moderating fluid intake, bladder retraining

333
Q

Second line treatment predominantly overactive bladder symptoms men

A

Anti muscarinic drugs - oxybutynin, tolterodine, darifenacin

334
Q

Third line treatment predominantly overactive bladder symptoms men

A

Mirabegron

335
Q

Treatment options nocturia in men

A

Moderating fluid intake at night
Furosemide 40mg late afternoon
Desmopressin

336
Q

Adverse effects suxamethonium

A

Hyperkalaemia
Malignant hyperthermia
Lack of acetylcholinesterase

337
Q

Adverse effects atracurium

A

Facial flushing
Tachycardia
Hypotension

338
Q

What nerve injury posterior triangle lymph node biopsy

A

Accessory nerve

339
Q

What nerve injury Lloyd Davies stirrups

A

Common peroneal nerve

340
Q

What nerve injury thyroidectomy

A

Laryngeal nerve

341
Q

What nerve injury anterior resection of rectum

A

Hypogastric autonomic nerves

342
Q

What nerve injury axillary node clearance

A

Long thoracic nerve, thoracodorsal nerve, intercostobrachial nerve

343
Q

What nerve injury inguinal hernia surgery

A

Ilioinguinal nerve

344
Q

What nerve injury varicose vein surgery

A

Sural and saphenous vein

345
Q

What nerve injury posterior approach to hip

A

Sciatic nerve

346
Q

What nerve injury carotid endarterectomy

A

Hypoglossal nerve

347
Q

Features acute limb threatening ischaemia

A

Pale
Pulseless
Painful
Paralysed
Paresthetic
Cold

348
Q

Initial management acute limb threatening ischaemia

A

Analgesia - IV opioids
IV unfractionated heparin - prevent propagation, particularly it not suitable for immediate surgery

349
Q

Definitive management options acute limb threatening ischaemia

A

Intra-arterial thrombolysis
Surgical embolectomy
Angioplasty
Bypass surgery
Amputation (if irreversible ischaemia)

350
Q

Features intermittent claudication

A

Aching or burning in leg muscles following walking - typically predictable distance before symptoms start, usually relieved within minutes of stopping, not present at rest

351
Q

First line investigation intermittent claudication

A

Duplex USS

352
Q

Investigation prior to intervention intermittent claudication

A

Magnetic resonance angiography MRA

353
Q

Interpretation of ABPI

A

1 normal
0.6-0.9 claudication
0.3-0.6 rest pain
<0.3 impending ischaemia

354
Q

Non-surgical management peripheral arterial disease

A

Quit smoking
Treat co-morbidities, e.g. hypertension, diabetes, obesity
Atorvastatin 80mg
Clopidogrel
Exercise training

355
Q

Treatment severe PAD/critical limb ischaemiar

A

Endovascular or surgical revascularisation

356
Q

Indications endovascular revascularisation PAD/critical limb ischaemia

A

Short segment stenosis (<10cm)
Aortic iliac disease
High risk patients

357
Q

Surgical techniques severe PAD/critical limb ischaemia

A

Surgical bypass with autologous vein/prosthetic material or endarterectomy

358
Q

Indications surgical revascularisation severe PAD/critical limb ischaemia

A

Long segment lesions (>10cm)
Multifocal lesions
Lesions of common femoral artery
Purely infrapopliteal disease

359
Q

Drugs used in peripheral artery disease

A

Naftidrofuryl oxalate - sometimes used for patients with poor quality of life

360
Q

Role of amputation in peripheral artery disease

A

Only in patients with critical limb ischaemia not suitable for other interventions such as angio or bypass surgery

361
Q

Causes priapism

A

Idiopathic
Sickle cell disease, other haemoglobinopathies
Erectile dysfunction medication, e.g. sildenafil, other PDE-5 inhibitor
Trauma
Drugs - cocaine, cannabis, ecstasy

362
Q

Features suggestive of non ischaemic priapism

A

Non painful erection or erection that is not fully rigid
History of trauma to genital region or perineal region

363
Q

Investigations priapism

A

Cavernosal blood gas analysis
Dopper or duplex ultrasonography (assess for blood flow in penis)
FBC and tox screen

364
Q

Interpretation cavernosal blood gas in priapism

A

In ischaemic priapism, pO2 and pH reduced, pCO2 increased

365
Q

First line treatment ischaemic priapism

A

If >4 hours, aspiration of blood from cavernosa combined with injection of saline flsuh to clear viscous blood that has pooled

366
Q

Second line treatment ischaemic priapism

A

Intracavernosal injection of vasoconstrictive agent such as phenylephrine, repeat at 5 minute intervals

367
Q

Third line treatment ischaemic priapism

A

Consider surgical options

368
Q

Treatment non-ischaemic priapism

A

Not medical emergency, normally suitable for observation as first line option

369
Q

Pathophysiology non-ischaemic priapism

A

Due to high arterial inflow, typically due to fistula formation often either as a result of congenital or traumatic mechanisms

370
Q

DRE findings prostate cancer

A

Asymmetrical, hard, nodular enlargement with loss of median sulcus

371
Q

First line investigation prostate cancer

A

Multiparametric MRI

372
Q

Interpretation of multiparametric MRI for prostate cancer

A

Results reported using 5-point Likert scale - if ≥3, prostate biopsy. If score 1-2, d/w patients pros and cons of having biopsy

373
Q

Complications TRUS prostate biopsy

A

Sepsis
Pain
Fever
Haematuria and rectal bleeding

374
Q

Who should have PSA testing

A

Men with suspected prostate cancer
Men older than 50 who ask for PSA test

375
Q

PSA level for referral <40

A

Use clinical judgement

376
Q

PSA level for referral 40-49

A

> 2.5

377
Q

PSA level for referral 50-59

A

> 3.5

378
Q

PSA level for referral 60-69

A

> 4.5

379
Q

PSA level for referral 70-79

A

> 6.5

380
Q

PSA level for referral >79

A

Use clinical judgement

381
Q

Causes for PSA rise

A

BPH
Prostatitis and UTI
Ejaculation
Vigorous exercise
Urinary retention
Instrumentation of urinary tract

382
Q

How long to wait to test PSA after prostatitis/UTI treatment

A

6 weeks

383
Q

How long to wait to test PSA after ejaculation

A

48 hours

384
Q

How long to wait to test PSA after vigorous exercise

A

48 hours

385
Q

Preferred method for detecting free air in abdomen

A

CT

386
Q

Most common histological subtype renal cell cancer

A

Clear cell

387
Q

Risk factors renal cell cancer

A

Middle age men
Smoking
Von Hippel-Lindau syndrome
Tuberous sclerosis

388
Q

Features renal cell cancer

A

Classic triad:
- Haematuria
- Loin pain
- Abdominal mass

Pyrexia of unknown origin
Endocrine effects
Paraneoplastic hepatic dysfunction syndrome
Varicocele
Stauffer syndrome

389
Q

Endocrine effects of renal cell cancer

A

May secrete:
- EPO → polycythaemia
- PTH related protein → hypercalcaemia
- Renin
- ACTH

390
Q

Features varicocele in renal cell cancer

A

Majority left sided
Caused by tumour compressing veins

391
Q

What is Stauffer syndrome

A

Paraneoplastic syndrome associated with renal cell cancer, typically presents with cholestasis/hepatosplenomegaly, thought to be due to raised IL-6

392
Q

Management renal cell cancer - confined

A

Partial or total nephrectomy

393
Q

Other treatments used in renal cell cancer

A

Alpha-interferon and IL-2 - used to reduce tumour size and treat mets

394
Q

Analgesic of choice renal colic

A

Diclofenac

395
Q

Analgesic if diclofenac not suitable/ineffective

A

IV paracetamol

396
Q

Role alpha blockers in renal stones

A

Consider for distal ureteric stones less than 10mm in size

397
Q

Imaging renal stones

A

Non-contrast CT KUB

398
Q

How quickly CT KUB in renal stones

A

If fever, solitary kidney, or diagnostic uncertainty, immediately
Otherwise, within 24 hours of admission

399
Q

Role of ultrasound renal stones

A

Used in pregnant women and children

400
Q

Management of renal stones

A

Watchful waiting if <5mm and asymptomatic
5-10mm shockwave lithotripsy
10-20mm shockwave lithotripsy or uteroscopy
>20mm percutaneous nephrolithotomy

401
Q

Management ureteric stones

A

<10mm - shockwave lithotripsy +/- alpha blockers
10-20mm ureteroscopy

402
Q

Indications for intervention in stones <5mm

A

Ureteric obstruction
Renal developmental abnormality, e.g. horseshoe kidney
Previous renal transplant

403
Q

Management ureteric obstruction due to stones with infection

A

Urgent surgical decompression - nephrostomy tube placement, insertion of ureteric catheters, ureteric stent placement

404
Q

Risks with shockwave lithotripsy

A

Solid organ injury from shockwaves
Fragmentation of larger stones → ureteric obstruction
Uncomfortable - needs analgesia during and after

405
Q

Indications for ureteroscopy in renal stones

A

For people where lithotripsy contraindicated, e.g. pregnant women, and complex stone disease

406
Q

What happens in ureteroscopy

A

Uretoscope pased thrgouh ureter and into renal pelvis. In most cases, stent left in situ for 4 weeks after procedure

407
Q

What happens in percutaneous nephrolithotomy

A

Access gained to renal collecting system, then intra corporeal lithotripsy or stone fragmentation performed and stone fragments removed

408
Q

Prevention of calcium renal stones

A

High fluid intake
Add lemon juice to water
Avoid carbonated drinks
Limit salt intake
Potassium citrate
Thiazide diuretics

409
Q

Prevention oxalate renal stones

A

Cholestyramine
Pyridoxine

410
Q

Prevention uric acid stones

A

Allopurinol
Urinary alkalinsation, e.g. oral bicarb

411
Q

Class I shock parameters

A

<750ml blood loss (<15%)
HR <100, BP normal
RR 14-20
UO >35ml/hr

412
Q

Class II shock parameters

A

750-1500ml blood loss (15-30%)
HR >100, BP normal
RR 20-30
UO 20-30ml/hr
Anxious

413
Q

Class III shock parameters

A

1500-2000ml blood loss (30-40%)
HR >120, BP decreased
RR 30-40
UO 5-15ml/hr
Confused

414
Q

Class IV shock parameters

A

> 2000ml blood loss (>40%)
HR >140, BP decreased
RR >35
UO <5ml/hr
Lethargic

415
Q

Causes of shock in trauma patients

A

Haemorrhage (most likely)
Tension pneumothorax
Spinal cord injury
Myocardial contusion
Cardiac tamponade

416
Q

What arterial pressure required to generate palpable femoral pulse

A

> 65mmHg

417
Q
A
418
Q

Hb target in haemorrhage

A

70-80 if no risk factors for tissue hypoxia
100 if risk factors

419
Q

Pathophysiology neurogenic shock

A

Spinal cord transection (usually) results in interruption to autonomic nervous system → decreased sympathetic tone or parasympathetic tone → decrease in peripheral vascular resistance mediated by marked vasodilation

420
Q

Treatment neurogenic shock

A

Peripheral vasoconstrictors

421
Q

Causes cardiogenic shock

A

In medical - ischaemic heart disease
In trauma - direct myocardial trauma or contusion

422
Q

Treatment cardiogenic shock

A

Largely supportive
TTE to look for pericardial fluid or direct myocardial injury
Sometimes need surgical repair

423
Q

What kind of trauma → cardiogenic shock is more likely to need surgical repair

A

Blunt trauma - right side of heart more likely to be affected with chamber and/or valve rupture

424
Q

What might be required as bridge to surgery in cardiogenic shock caused by trauma requiring repair

A

Intra-aortic balloon pump

425
Q

AXR SBO

A

Distended small bowel loops (>3cm) with fluid levels

426
Q

Causes SAH

A

Head injury (most common)
Intracranial aneurysm (berry aneurysms)
Arteriovenous malformation
Pituitary apoplexy
Mycotic (infective) aneurysms

427
Q

Conditions associated with berry aneurysms

A

Hypertension
Adult PKD
Ehlers-Danlos syndrome
Coarctation of the aorta

428
Q

ECG changes SAH

A

ST elevation

429
Q

First line investigation SAH

A

Non-contrast CT head

430
Q

Findings non-contrast CT head in SAH

A

Acute blood (hyperdense/bright) typically distributed in basal cisterns, sulci, and in severe cases ventricular system

431
Q

When to do LP in SAH

A

If CT head done more than 6 hours from symptom onset and is normal. LP should be done at least 12 hours from symptom onset (allow time for development of xantochromia)

If CT head done within 6 hours of symptom onset and normal, no LP

432
Q

LP findings SAH

A

Xanthochromia
Normal or raised opening pressure

433
Q

Investigations in confirmed SAH

A

CT intracranial angiogram
+/- digital subtraction angiogram (catheter angio)

434
Q

Supportive management SAH

A
  • Bed rest
  • Analgesia
  • VTE prophylaxis
  • Discontinuation of antithrombotics (reversal if anticoagulated)
435
Q

Drug treatment SAH

A

Nifedipine - prevent vasospasm

436
Q

Indications for surgery SAH

A

SAH caused by intracranial aneurysms - risk of rebleeding, so ideally within 24 hours

437
Q

Surgical options aneurysmal SAH

A

Most treated with coiling by IR
Minority need craniotomy and clipping by neurosurg

438
Q

Complications aneurysmal SAH

A

Re-bleeding
Hydrocephalus
Vasospasm (delayed cerebral ischaemia)
Hyponataemia
Seizures

439
Q

When does re-bleeding occur aneurysmal SAH

A

Most common in first 12 hours

440
Q

Presentation re-bleeding aneurysmal SAH

A

Sudden worsening of neurological symptoms

441
Q

Investigation rebleeding aneurysmal SAH

A

Repeat CT head

442
Q

Treatment hydrocephalus secondary to aneurysmal SAH

A

External ventricular drain
Sometimes needs long term VP shunt

443
Q

When does vasospasm occur aneurysmal SAH

A

7-14 days after onset

444
Q

Management vasospasm after aneurysmal SAH

A

Euvolaemia
Vasopressor

445
Q

Cause hyponatraemia aneurysmal SAH

A

Most likely SIADH

446
Q

Timeframe acute subdural haemorrhage

A

Symptoms within 48 hours of injury, rapid neurological deterioration

447
Q

Timeframe subacute subdural haemorrhage

A

Days to weeks post-injury, gradual progression

448
Q

Timeframe chronic subdural haemorrhage

A

Weeks to months, may not recall specific injury

449
Q

Classic presentation SDH

A

Head trauma (minor to severe) → lucid interval → gradual decline in consciousness

450
Q

Neurological symptoms SDH

A

Altered mental status - range from mild confusion to deep coma, fluctuations common
Focal neurological deficit - weakness on one side of body, aphasia, visual field defects
Headache - localised to one side, worsen over time
Seizures

451
Q

Physical examination findings SDH

A

Papilloedema
Pupil changes - unilaterally dilated pupil on side of haematoma (compression of CN 3)
Gait abnormality - ataxia, unilateral weakness
Hemiparesis/hemiplegia

452
Q

Behavioura/cognitive change SDH

A

Memory loss (esp in chronic)
Perosnality changes - irritability, apathy, depression
Cognitive impairment - difficulty with attention, problem solving, other executive functions

453
Q

CT findings acute SDH

A

Crescenteric collection, not limited by suture lines, hyperdense
Large SDH cause midline shift/herniation

454
Q

Management acute SDH

A

Small/incidental SDH observed conservatively
Surgical options - monitoring ICP, decompressive craniectomy

455
Q

Cause chronic SDH

A

Rupture of small bridging veins within subdural space, causing slow bleeding

456
Q

Risk factors chronic SDH

A

Elderly
Alcoholic

Brain atrophy → fragile or taut bridging veins

457
Q

Presentation chronic SDH

A

Weeks to months progressive confusion, reduced consciousness, neuro deficit

458
Q

CT findings chronic SDH

A

Crescenteric shape not restricted by suture lines, HYPOdense (dark) - in contrast to acute

459
Q

Management chronic SDH

A

If incidental or small, conservative management
If confused, associated neuro deficit, or severe imaging findings - surgical decompression with burr holes

460
Q

Management superficial thrombophlebitis

A

NSAIDs - topical mild, oral more severe
Topical heparinoids in superficial
Compression stockings
Low molecular weight heparin

461
Q

Investigation superficial thrombophlebitis

A

If affects proximal long saphenous vein, should have USS to exclude concurrent DVT

462
Q

Investigation prior to compression stockings

A

ABPI

463
Q
A

1 - MSRA (17 decks)

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