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Junior Surgery > Abdo Pain And Jaundice > Flashcards

Abdo Pain And Jaundice Flashcards

1
Q

What is inflammatory pain indicative of in the acute abdomen

A

Peritonitis - inflammation of peritoneum - gives localised pain
Constant pain, with a raised temp, pulse and leucocytosis

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2
Q

What is obstructive pain indicative of in the acute abdomen

A

Colicky pain, often agitated
Pain may become constant with superimposed inflammation

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3
Q

What is referred visceral pain indicative of in the acute abdomen

A

Foregut - oseophagus to D2 pain is referred to upper abdo
Midgut - D2 to transverse colon is referred to middle abdo
Hindgut pain is referred to lower abdo

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4
Q

Vascular differentials of the acute abdomen

A

AAA
Mesenteric thrombosis / embolus

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5
Q

Visceral differentials of the acute abdomen

A

Acute appendicitis
Meckel’s diverticulitis
Intestinal obstruction
Perforated viscus
Acute pancreatitis
Acute cholecystitis
Renal calculi
The acute scrotum
IBD

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6
Q

Medical differentials of the acute abdomen

A

GORD
Referred pain from pneumonia / MI / UTI / pyelonephritis

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7
Q

Gynae causes of the acute abdomen

A

Ruptured ectopic
Torted / ruptured ovarian cysts
Salpingitis

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8
Q

Essential investigations for the acute abdomen

A

FBC, U&E, LFTs, CRP, lipase and blood gas
Pregnancy test
Urinalysis
Imaging

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9
Q

What is a CT abdomen / pelvis used for

A

Diagnostic for most surgical pathologies

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10
Q

What is an erect CXR used for

A

Useful if suspecting perforated viscus

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11
Q

What is an US used for in acute abdomen

A

Most useful if suspecting gynae pathology or biliary pathology

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12
Q

What is acute appendicitis

A

Occurs when the appendix lumen is obstructed by a faecolith, foreign body or lymphoid enlargement in the wall
Bacteria can then proliferate in the obstructed loop of bowel eventually leading to necrosis and perforation due to raised intraluminal pressure
Most commonly occurs in ages 10-30

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13
Q

Symptoms of acute appendicitis

A

Abdo pain - starts dull and central then becomes localised and sharp in RIF
Anorexia
N&V

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14
Q

Signs of acute appendicitis

A

Tachycardia
Mild fever, flushing and fetor
RIF tenderness / guarding
Rebound + percussion tenderness in RIF
Rosving’s sign (more painful in RIF than LIF when LIF pressed)
Psoas sign (pain on R hip extension: retroperitoneal retrocaecal appendix)
Obturator sign (pain on internal rotation of R hip)

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15
Q

Imaging used in suspected acute appendicitis

A

In females of child bearing age US is used to try and rule out gynae pathology

In older patients CT abdo / pelvis is used to rule out alternate surgical pathology

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16
Q

Management of acute appendicitis

A

ABCDE resuscitation including IV abx
Laparoscopic appendectomy

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17
Q

Early / late complications of laparoscopic appendectomy

A

Early: haematoma / wound infections
Late: small bowel obstruction or incisional hernia

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18
Q

Complications of acute appendicitis perforation

A

Peritonitis and sepsis
Appendiceal mass - inflamed appendix becomes covered with omentum
Appendiceal abscess - local / pelvic / subhepatic / subphrenic
Adhesions

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19
Q

Pathophysiology of gallstone disease

A

Bile usually contains cholesterol, phospholipids, bile salts, water and conjugated bilirubin
Bile flows into the gallbladder if the sphincter of oddi is closed where it becomes more concentrated as water is absorbed
Presence of fatty acids or amino acids in the duodenum will lead to release of CCK which causes the gall bladder to contract and bile to be released

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20
Q

What is cholelithiasis

A

Formation of stones in the gallbladder

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21
Q

What are cholesterol gallstones

A

Cholesterol crystallisation within the gall bladder bile due to excess cholesterol secretion into the bile or loss of bile salt content

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22
Q

Cholesterol gallstone risk factors

A

Increasing age
Obesity, high fat diet, rapid weight loss
Female sex, multiparity, pregnancy, OCP
DM
Ileal disease
Liver cirrhosis

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23
Q

What are bile pigment stones

A

Both black and brown pigment gallstones contain calcium bilirubinate and form independently of cholesterol stones
- black is associated with haemolytic conditions
- brown occur due to biliary stasis / infection

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24
Q

What is the difference between biliary colic and cholecystitis

A

Both are formed by cholelithiasis
Biliary colic - no associated inflammation / infection
Cholecystitis - associated inflammation / infection

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25
Q

What is choledocholithiasis

A

Stone impactation in the common bile duct
Can cause biliary colic if temporary or painful obstructive jaundice if more prolonged
Can also predispose to ascending cholangitis or acute pancreatitis

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26
Q

What is gallstone ileus

A

Uncommon
Large gallstone erodes through to the gall bladder and into adjacent duodenum
- then can produce an obstruction if it impacts in a narrow segment of bowel

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27
Q

How does gallstone ileus appear on CT / X-ray

A

Signs of small bowel obstruction
The gallstone may be visible and there will be air in the biliary tree

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28
Q

What is biliary colic

A

Associated with temporary obstruction of the gallbladder, cystic duct or common bile duct due to gallstones

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29
Q

Symptoms of biliary colic

A

Severe constant epigastric / RUQ pain with a crescendo characteristic
May radiate to back or right shoulder / subscapular region
N&V
Worse upon food consumption (fatty)
Systemically well

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30
Q

What is acute cholecystitis

A

Obstruction of gall bladder emptying (usually due to gall stone)
Leads to gall bladder distension
There is ongoing water reabsorption from the retained bile which becomes highly concentrated leading to inflammatory response in wall of gallbladder

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31
Q

Features of acute cholecystitis

A
  • severe localised RUQ pain
  • vomiting and systemic upset
  • palpable gall bladder - Murphy sign positive
  • rarely the gall bladder can become gangrenous and perforate leading to generalised peritonitis
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32
Q

What is ascending cholangitis

A

Infection of the common bile duct which usually occurs following obstruction due to choledocholithiasis

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33
Q

Symptoms of ascending cholangitis

A

Obstructive jaundice
High fever
RUQ pain

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34
Q

What is the key presentation of all forms of gall stone disease

A

RUQ pain

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35
Q

Blood results in biliary colic

A

Normal

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36
Q

Blood results in cholecystitis

A

Raised inflammatory markers (WCC / CRP)
LFTs may show marginal derangement

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37
Q

Blood results in choledocholithiasis

A

Normal inflammatory markers
Obstructive jaundice type picture on LFT (high bilirubin, raised ALP/ GGT)

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38
Q

Blood results in ascending cholangitis

A

Raised inflammatory markers
Obstructive jaundice on LFTs

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39
Q

US findings in biliary colic

A

Stones in gall bladder (echogenic foci and acoustic shadow)

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40
Q

US findings in cholecystitis

A

Thickened gall bladder wall in acute inflammation

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41
Q

US findings in choledocholithiasis / ascending cholangitis

A

Increased diameter of the common bile duct in obstruction

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42
Q

When is MRCP used (magnetic resonance cholangiopancreatography)

A

When there is diagnostic uncertainty or concern about underlying malignancy
Can visualise the biliary tree in greater detail

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43
Q

Management of asymptomatic gallstones (found incidentally)

A

Cholecystectomy only indicated if the patient is at significant risk of complications due to co-morbidities

  • young patients also indicated as there is a long time for symptoms to develop
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44
Q

Management of biliary colic

A

Oral analgesia
Elective laparoscopic cholecystectomy
Low fat diet

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45
Q

Management of acute cholecystitis

A

Bed rest, fluids, analgesia
IV abx
Laparoscopic cholecystectomy

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46
Q

Management of choledocholithiasis

A

Bed rest, fluids, analgesia
Inpatient ERCP
Upper GI endoscopy with cannulation of common bile duct via sphincter of oddi
Obstructing stones broken down and removed
IV vit K to aid coagulation
Laparoscopic cholecystectomy following relief of obstruction / jaundice

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47
Q

Management of ascending cholangitis

A

Sepsis 6 with urgent IV abx and emergency ERCP
Patients with an infected, obstructed biliary system are high risk of rapid deterioration

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48
Q

Define acute pancreatitis

A

An acute inflammation of the pancreas which can be associated with significant morbidity and mortality

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49
Q

Pathology of acute pancreatitis

A

An initial insult to the pancreas leads to leakage of activated pancreatic enzymes into the pancreatic and peripancreatic tissue causing an acute inflammatory reaction eg gall stones damaging ampulla of vater which allows gastric contents up the pancreatic duct where they can activate pro enzymes

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50
Q

Acute pancreatitis aetiology (I GET SMASHED)

A

Idiopathic (20%)
Gall stones (40%)
Ethanol (35%)
Trauma (15%)
Steroids
Mumps (+CMV +EBV)
Autoimmune
Scorpion venom
Hyper / hypo lipidaemia, calcaemia, thermos
ERCP
Drugs (thiazides, sulphonamides, ACEIs, NSAIDs)

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51
Q

Symptoms of acute pancreatitis

A

Severe epigastric pain
Radiates to the back and may be relieved by sitting forward
N&V

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52
Q

Signs of acute pancreatitis

A

Tachycardia
Fever
Ileus
Jaundice
Rigid abdomen
Cullens sign (periumbilical discolouration due to peritoneal haemorrhage)
Grey-turner’s sign: flank discolouration

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53
Q

What is bruising in pancreatitis a sign of

A

Grave prognosis (80% mortality)

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54
Q

Investigations for acute pancreatitis

A

Bloods: FBC, CRP, U&E, LFT, glucose, calcium, raised serum lipase, ABG

ECG: to rule out MI

Imaging: erect CXR, RUQ US, CT abdo, MRCP

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55
Q

How to diagnose pancreatitis

A

Classic clinical history + raised serum lipase is enough without imaging

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56
Q

What is ALT >3x normal suggestive of

A

Gallstone disease

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57
Q

What is the modified Glasgow criteria for assessing severity of pancreatitis (PANCREAS)

A

PaO2 <8kPa
Age >55
Neutrophils: WBC >15x10^9
Calcium: <2mmol/L
Renal: urea >16mmol/L
Enzymes: LDH >600iu/L, AST >200iu/L
Albumin: <32g/L
Sugar: glucose >10mmol/L

Score of 3 or above suggest severe pancreatitis (HDU/ITU)

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58
Q

Management of pancreatitis

A

ABCDE for initial resuscitation
Aggressive IV fluid
Catheterise and monitor urine output
Analgesia
PPI to prevent stress ulcer
DVT prophylaxis
Urgent ERCP if due to gallstones
Withhold offending medications

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59
Q

Early complications of acute pancreatitis

A
  • shock (hypovolemic, septic)
  • ARDS
  • renal failure
  • DIC
  • metabolic: Hypocalcaemia, hyperglycaemia, hypalbuminaemia
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60
Q

Late complications of acute pancreatitis

A

Abscess formation
Pancreatic pseudocysts
Intra-abdominal haemorrhage
Thrombosis of the splenic / gastroduodenal arteries
Fistulae

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61
Q

What is a pancreatic pseudocyst

A

A localised fluid collection rich in pancreatic enzymes with a non-epithelialised wall containing fibrous / granulation tissue

Commonly occur in pancreatitis from day 10 onwards due to disruptions of the pancreatic duct leading to extravasation of enzymes

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62
Q

How does a pancreatic pseudocyst present

A

Deep persistent abdominal pain +/- a mass

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63
Q

Acute pancreatitis prognosis

A

85% of cases settle after 3-7 days
15% require ICU admission
50% of ICU cases will end in mortality

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64
Q

Define an aneurysm

A

A focal dilation of an artery >150% of its normal diameter

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65
Q

What is a true aneurysm

A

All layers of the arterial wall are involved

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66
Q

What is a false aneurysm / pseudoaneurysm

A

Surrounding soft tissues lined by thrombus form the wall of the aneurysm, mainly occurring following trauma

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67
Q

AAA presentations

A

Mass effects: pressuring adjacent structures
Emboli events: due to development of mural thrombi
Haemorrhage: due to rupture

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68
Q

AAA causes

A

Atherosclerotic: eg aortic, popliteal
Developmental: berry aneurysm
Infective: mycotic in endocarditis, syphilitic in tertiary syphilis
Developmental: Marfaans / ehlers-Danlos syndrome
Trauma

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69
Q

Presentation of AAA rupture

A
  • severe continuous / intermittent epigastric pain radiation to the back / groin
    -pulsatile, expansile abdominal mass
  • signs of shock
  • AAA should be suspected in any male >50 presenting with renal colic
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70
Q

Management of AAA

A

Emergency A-E resuscitation
Transfusion for rapid blood delivery
Patient taken to theatre when stabilised
Clamp aorta bone the leak then graft

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71
Q

Prognosis of AAA

A

Only 50% make it to hospital
Of these 50% will not survive the operation

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72
Q

Management of AAA <5.5cm

A

Monitor by regular US / CT every 6-12 months
Strict control of HTN
Smoking cessation

73
Q

What types of monitored AAA are indicated for surgery

A

> 6cm as risk of rupture increases to 25%
AAA expanding at >1cm/year
Symptomatic

74
Q

Which types of AAA patients are at more of a risk of rupture

A

Hypertension
FH of rupture
Smokers
Females

75
Q

Describe an endovascular aneurysm repair

A

Use of femoral arteries to access and stent the aorta under fluoroscopic guidance
- lower mortality than conventional open operation
- lower post operative morbidity

76
Q

Why is CKD a risk in AAA repair

A

The contrast used in EVAR’s is nephrotoxic
In an open procedure there is a prolonged ischaemia to the kidneys after the aorta is clamped

77
Q

Complications of popliteal aneurysms

A

Acute limb ischaemia: due to rupture / thrombosis of the aneurysm or distal emboli
Chronic limb ischaemia: gradual occlusion of the aneurysm
DVT: if occluding popliteal veins

78
Q

Investigations in popliteal aneurysms

A

USS to determine the size of the aneurysm
Angiography prior to the surgery to assess the distal arterial tree

79
Q

Management of popliteal aneurysm

A

Femoral to distal popliteal bypass graft
Intra-vascular thrombolysis or embolectomy may occur at the time of surgery for the distal emboli

80
Q

What is peritonitis

A

Inflammation of the peritoneum
Generally related to an underlying surgical pathology

81
Q

Anatomy of the peritoneum

A

Is made up of the parietal peritoneum (above abdominal cavity) and visceral peritoneum (lines intraperitoneal organs)
The potential space between the 2 layers is known as the peritoneal cavity

82
Q

What is localised peritonitis

A

Inflammation of the intra-abdominal organs will lead to localised inflammation of the peritoneum overlying that particular organ eg appendicitis, cholecystitis

83
Q

What is generalised peritonitis

A

GI perforation (or ruptured reproductive organs / ectopic pregnancy) can cause widespread peritoneal inflammation and generalised peritonitis
- initially chemical due to the acidic nature of GI contents but infection invariably develops after 24-48 hours

84
Q

Peritonitis presentation

A

Sudden onset abdominal pain - worse on movement
Generalised peritonitis - washboard rigidity
Localised peritonitis - guarding of affected area
Fever
Signs of shock (tachycardia / hypotension)
Sepsis

85
Q

Aetiology of peritonitis

A

Abdo organ inflammation
Perforated GI viscus
Post surgical / post trauma
Spontaneous bacterial peritonitis - in ascitic fluid in liver failure and ascites

86
Q

Investigations for peritonitis

A

CT abdomen / pelvis

87
Q

Management of peritonitis

A

ABCDE resuscitation
Broad spectrum IV abx
Surgical management if underlying cause is surgical

88
Q

What is GI perforation

A

Linked to peritonitis
Most commonly seen as a complication of other intra-abdominal pathologies
Requires full thickness injury of the bowel wall

89
Q

Aetiology of GI perforation

A
  • instrumentation (endoscopy, surgical)
  • trauma
  • bowel obstruction
  • malignancy
  • appendicitis
  • PUD
  • Diverticular disease
  • IBD
  • severe constipation
  • violent vomiting
90
Q

Describe localised GI perforation

A

Inflammatory response at the site of the perforation and the GI contents become walled off by the immune system leading to abscess formation
- diffuse spread of GI contents throughout the abdomen, leading to diffuse peritonitis

91
Q

GI perforation presentation

A

Acute severe abdo pain
Pts who do not present with pain at the time of perforation will develop infection secondary to contamination of the abdomen and present with sepsis

92
Q

OE of GI perforation

A

Guarding and rigidity
Appear toxic
Sepsis in localised

93
Q

Investigations for GI perforation

A

Bloods:
- raised inflammatory markers (WCC, CRP)
- raised lactate if developing shock
- take coagulation profile and group and save as most require theatre

Imaging:
- upright CXR / AXR: pneumoperitoneum
- CT abdo / pelvis: free gas / fluid in abdo and perforated viscus

94
Q

Management of GI perforation

A

ABCDE resuscitation
Broad spectrum IV abx
Usually requires surgical exploration

95
Q

Define shock

A

Acute circulatory failure that compromises tissue perfusion
Can lead to irreversible organ damage and death due to cellular hypoxia

96
Q

What is hypovolemic shock

A

Shock due to a lack of intravascular volume
- haemorrhage
- dehydration

97
Q

What is distributive shock

A

Shock due to severe peripheral vasodilation
- sepsis
- anaphylaxis
- neurogenic shock - inhibition of spinal cord sympathetic outflow leading to vasodilation

98
Q

What is cardiogenic shock

A

Shock due to intracranial causes of cardiac pump failure
- MI, arrhythmias, valve dysfunction, metabolic disturbances

99
Q

What is obstructive shock

A

Shock due to extra cardiac causes of cardiac pump failure
- Massive PE, cardiac tamponade, tension pneumothorax

100
Q

Clinical features of hypovolemic / cardiogenic shock

A

Patient is cold, pale, clammy with rapid threads pulse
Pulse pressure low due to vasoconstriction

101
Q

Clinical features of septic shock

A

Patient is flushed, hot, sweaty, rapid bounding pulse
Pulse pressure wide due to vasodilation

102
Q

Effect of shock on cerebral system

A

Autoregulation with mean arterial pressure of 50-150mmHg but below this the patient will become agitated, confused, drowsy and unresponsive

103
Q

Effect of shock on cardiac system

A

Reduced diastolic pressure leads to inadequate myocardial perfusion leading to ischaemic chest pain, arrhythmias, and infarction

104
Q

Effects of shock on respiratory system

A

Increased resp rate to compensate for metabolic acidosis secondary to tissue hypoperfusion

105
Q

Effects of shock on renal system

A

Autoregulation with MAP of 70-170mmHg but below this there will be oliguria which leads to impaired renal function due to toxin build up

106
Q

Effects of shock on GI system

A

Decreased gut motility and nutrient absorption, and decreased ability to sustain normal flora, leading to infection susceptibility

107
Q

Effect of shock on skin

A

Blood supply is centralised giving cool / clammy / mottled peripheral skin

108
Q

Define sepsis

A

The body’s overwhelming response to infection that can lead to tissue damage, organ failure and death

109
Q

Pathophysiology of sepsis

A

Excessive cytokine release leads to a cascade of cellular changes that cause vasodilation, increased vascular permeability, immune system impairment and inappropriate activation of the coagulation cascade

110
Q

High risk criteria for sepsis

A

Behaviour: objective evidence of new alteration in mental state
HR: >130 bpm
RR: >25 or new oxygen saturation requirement
SBP: <90mmHg or more than 40 below baseline
Urine output: not passed urine in previous 18 hours or less than 0.5ml/kg urine per hour in catheter
Skin: mottled appearance or cyanosis or non blanching rash

111
Q

Moderate risk criteria for sepsis

A

Behaviour: new onset altered behaviour or history of acute deterioration in function
HR: 91-130bpm
RR: 21-25
SBP: 91-100 mmHg
Urine output: not passed urine in the past 12-18hrs or for catheterised patients passed 0.5-1ml/kg of urine per hour

112
Q

Define severe sepsis

A

Sepsis + hypotension or evidence of end organ dysfunction
Eg oliguria, confusion, lactate >2, SpO2<94%

113
Q

Define septic shock

A

Severe sepsis with hypotension not responding to fluid resuscitation

114
Q

What are the sepsis 6 (3 in, 3 out)

A
  1. Oxygen (in): 15ml/min via a non rebreather mask to achieve >94% sats (88-92 in COPD)
  2. IV fluids (in): 500ml crystalloid stat if hypotensive or lactate >2
  3. IV abx (in): local guidelines
  4. Serum lactate (out): VBG or ABG. Seek urgent senior review if lactate >4
  5. Blood cultures (out): ideally prior to abx. Take 2 pairs from separate sites plus from all indwelling lines
  6. Catheterise (out): urine output is the most reliable measure of end organ perfusion
115
Q

Pathophysiology of anaphylactic shock

A

Type I IgE mediated hypersensitivity reaction occurring in response to an angiogenesis that the body has previously been sensitised to
Degranulation of mast cells leads to release of vasoconstrictive mediators such as histamine that cause excessive vasodilation of the venous system
Compounded by bronchoconstriction and laryngeal oedema

116
Q

Acute management of anaphylactic shock

A
  1. Secure airway (intubation)
  2. Remove cause
  3. Adrenaline 0.5mg IM every 5 mins if necessary
  4. Chlorphenamine 10mg IV
  5. Hydrocortisone 200mg IV
  6. If wheeze treat as per acute asthma
  7. Raise feet of bed to help restore circulation
  8. Interval bloods for serum tryptase and histamine to confirm diagnosis
117
Q

Management of hypovolaemic shock

A

ABCDE
- replace any fluids being lost and titration to HR / BP / CVP / urine output
- inotropes considered if persistently hypotensive

118
Q

Management of cardiogenic shock

A

ABCDE
IV diamorphine 2.5-5mg for pain / anxiety / breathlessness
Assess pulmonary oedema, don’t give fluids - furosemide infusion can provide relief
ITU / CCU for ionotropic support

119
Q

What is pelvic inflammatory disease

A

Inflammatory condition involving upper genital tract in women
Can involve all of the uterus, Fallopian tubes, ovaries and neighbouring pelvic organs

120
Q

Risk factors for PID development

A

Sexually active
Multiple partners
Age <25
Lack of barrier contraception
Previous STI / previous PID
IUD insertion

121
Q

How can IUD insertion cause PID

A

All patients should be screened for infection prior to IUD insertion as the IUD can introduce the infection from the lower genital tract to the upper

122
Q

Pathophysiology of PID

A

Endocervical canal usually forms a barrier between the vagina and upper vaginal tract
Endocervical infection can result in disruption of this barrier allowing vaginal bacteria to enter the upper genital tract
Variance between individuals can be due to immune response, oestrogen levels and cervical mucus

123
Q

Clinical features of PID

A

Lower abdo pain
Dyspareunia
Abnormal uterine bleeding
Abnormal cervical or vaginal discharge
Severe disease: fever, significant abdo pain, rebound tenderness

124
Q

OE of PID

A

Lower abdominal / pelvic tenderness
Purulent cervical discharge seen on speculum examination
Pelvic organ tenderness - cervical motion, uterine and adnexal tenderness

125
Q

Investigations for PID

A

Bloods: raised inflammatory markers
Vaginal discharge: send for MCS + PCR to identify infective organism
Screen for pregnancy, HIV, syphilis
USS to assess for abscess / adnexal pathology

126
Q

Management of PID

A

Abx 14 days
Broad spectrum due to polymicrobial nature

127
Q

Complications of PID

A

Perihepatitis - inflammation of liver capsule and peritoneal surfaces

Tubo-ovarian abscess - may have palpable adnexal mass on exam

Chronic PID - low grade fever, weight loss, abdo pain

Increased future risk of ectopic pregnancy secondary to fallopian tube damage

128
Q

Prognosis of PID

A

90% of cases resolve with simple abx therapy
Gonorrhoea infections are generally more severe and give higher rates of complications

129
Q

2 types of intestinal obstruction

A

Small bowel or large bowel

130
Q

How can vomiting indicate the type of intestinal obstruction

A

Vomiting:
- undigested food suggests gastric outlet obstruction
- bilious vomiting suggests upper SBO
- faeculent vomiting (thick / foul smelling) suggests more distal SBO / LBO

131
Q

Symptoms of intestinal obstruction

A

Vomiting
Abdo pain
- intense, colicky
- worsening may represent strangulation / perforation

Constipation - inc absence of passing wind.

132
Q

Signs of intestinal obstruction

A
  • abdo distension
  • minimal abdo tenderness (except bowel strangulation)
  • tinkling bowel sounds
  • dehydration - due to fluid accumulation
  • central resonance to percussion
  • scars : previous surgery causing adhesions
  • palpable mass
133
Q

Aetiology of SBO

A

Adhesions (80%)
Hernias
Crohn’s
Intussusception

134
Q

Aetiology of LBO

A

Carcinoma of the colon
Diverticular disease
Sigmoid volvulus
Constipation

135
Q

Investigations for intestinal obstruction

A

FBC, U&E, lipase, LFT, CRP
ABG / VBG : assess lactate - raised indicated bowel ischemia
Urinalysis / pregnancy test
CT abdo / pelvis can confirm diagnosis and indicate level of obstruction but will not show cause

136
Q

Management of SBO

A

ABCDE resuscitation
NBM +NG decompression of stomach
If no signs of strangulation delay operative management by 48 hrs
Gastrograffin follow through can show level of obstruction
Abx + surgery if strangulation

137
Q

Management of LBO

A

Operative (Hartmann’s)

138
Q

What is strangulation in intestinal obstruction

A

Occurs when a section of the bowel is cut off from its blood supply
Most commonly occurs with a volvulus or hernia however can occur in any obstruction
Suspect if there is increasing pain / tenderness with leucocytosis and systemic upset

139
Q

What is a volvulus

A

A twisting loop of bowel around its mesenteric axis resulting in obstruction +/- strangulation

140
Q

What is a sigmoid volvulus

A

Most common in elderly, constipated patients
Classic coffee bean appearance on X-ray
Treatment is insertion of a long flatus tube advanced into the sigmoid which often untwists the volvulus and releases large amounts of liquid faeces / gas
If unsuccessful - emergency laparotomy

141
Q

What is a caecal volvulus

A

Due to congenital malformation and gives the classic ‘embryo’ appearance of an ectopically placed caecum on an AXR
Treatment is untwisting at laparotomy

142
Q

What is a paralytic ileus

A

Temporary disruption of normal peristaltic activity of the small bowel without a mechanical blockage
No bowel sounds
Identifiable cause:
- post surgery
- intra-abdominal sepsis
- electrolyte disturbances
- critically unwell patients

143
Q

Treatment of paralytic ileus

A

NG tube and NBM

144
Q

Describe the pathway of pain

A

A delta fibres give rise to perception of sharp immediate pain
C fibres give rise to slower onset, prolonged pain
Sensory impulses enter the cord via the dorsal root, and then ascend in the dorsal posterior column or the spinothalamic tract
Thalamic pathways to and from the cortex then mediate the emotional components of pain

145
Q

Physiological effects of pain

A

Leads to catecholamines release with the resultant vasoconstriction leading to increased cardiac work and delayed healing

146
Q

Outline the WHO pain ladder

A
  1. Non-opioid +/- adjuvant eg paracetamol +/- NSAID
  2. Weak opioid +/- non opioid +/- adjuvant eg codeine + para + NSAID
  3. Strong opioid +/- non opioid +/- adjuvant eg morphine + para + NSAID
147
Q

MOA of paracetamol

A

Partially unknown
Acts similarly to NSAIDs
Inhibits CNS prostaglandin synthesis

148
Q

Properties of paracetamol

A

Good analgesic and antipyretic properties
Weak anti inflammatory

149
Q

When is a 3g/day max indicated in paracetamol

A

Old age
Poor nutritional status
Alcoholism

150
Q

How do NSAIDs work

A

Inhibit COX enzymes which normally promote production of prostaglandins and thromboxane

COX 1- expressed in most tissues with the PGs produced involved in tissue homeostasis - platelet aggregation, renal blood flow, Autoregulation and GI protection

COX 2 - induced in active inflammatory cells by IL-1 and TNF-a
Sensitises nociceptors to inflammatory mediators such as bradykinin peripherally
Sensitises afferent pain fibres in the dorsal horn centrally

151
Q

What unwanted effects does inhibiton of COX-1 (NSAIDs) lead to

A

Dyspepsia and gastric ulcers
Bronchospasm
Renal insufficiency
Cardiotoxicity
Decreased platelet count
Skin reactions

152
Q

Absolute contraindications for inhibiton of COX-1 (NSAIDs)

A

Severe heart failure
History of GI bleed / ulceration

153
Q

When should NSAIDs be cautioned

A

Asthma
Elderly
Coagulopathies
Renal / hepatic / cardiac impairment

154
Q

NSAID of choice for high CV risk

A

Naproxen

155
Q

When is Diclofenac contraindicated

A

CV disease or high risk of CV events

156
Q

Effective alternatives to oral NSAIDs

A

Topical NSAID gel effective for pain relief from arthritis
Topical capsaicin (chilli extract) can provide significant pain reduction if applied regularly 1-2 weeks

157
Q

What are coxibs

A

COX-2 selective inhibitors
- used in RA / OA but has risk of serious adverse cardiac events
PPI should still be co-prescribed

158
Q

How do opiates act

A

Act on u-opioid receptors in the CNS and throughout the body, decreasing neuro-excitability
Not effective in neuropathic pain

159
Q

Side effects of opiates

A

Respiratory depression
N+V
Constipation
Sedation / depression of cough reflex
Gall bladder contraction (avoid in gall stone disease)

160
Q

Absolute contraindications of opiates

A

Acute respiratory depression
Acute alcoholism
Risk of paralytic ileus
Raised ICP
Tramadol should not be used in conjunction with other serotonergic drugs
Tolerance develops within a few days - dependence may occur

161
Q

What to do in opiate overdose

A

IV naloxone can rapidly reverse the toxic effects of opiates

162
Q

What is co-prescribed for people on long term opiates

A

Senna
Lactulose

163
Q

Indications of patient controlled analgesia

A

Post operatively or in oncology

164
Q

Advantages of patient controlled analgesia

A

Allows for administration of patient controlled doses when required
Improves patient satisfaction and decreases overall doses used

165
Q

Examples of non-drug analgesia

A

Splinting: very effective analgesia technique in trauma
Cold therapy: very effective around joints post surgery
TENS: electrical current applied via hand held generator to activate nerve fibres in tissues below
Acupuncture: can be effective in certain conditions
CBT

166
Q

What is an indicator of severe disease in pancreatitis

A

Hypocalcaemia

167
Q

What do raised amylase and lipase indicate

A

Acute pancreatitis
Amylase : 3-4x the normal range
Lipase: more of a specific marker than amylase - does not predict severity

168
Q

What is the most sensitive blood test for diagnosis of acute pancreatitis

A

Serum lipase as has a longer half life whereas amylase levels can fluctuate and lead to false negative results

169
Q

What test should be used for suspected pancreatitis presenting >24 hours after onset

A

Serum lipase as has a longer half life

170
Q

How would a blockage of the cystic duct or gall bladder present

A

RUQ pain
No jaundice

171
Q

Why is Crohn’s disease a risk factor for gall stones

A

Affects the terminal ileum which is involved in metabolism of bile salts
Excessive bile salts escape into the colon, are reabsorbed and return to the liver resulting in excessive secretion of bile pigments and the production of black stones

172
Q

What is faecal elastase test used for in pancreatitis

A

Test of exocrine function of the pancreas

173
Q

Test done to investigate obstruction with ascending cholangitis

A

ERCP

174
Q

What is the name of the investigation for diagnosis and monitoring the severity of liver cirrhosis

A

Transient elastography

175
Q

Which antibodies are positive in primary sclerosing cholangitis

A

P - ANCA

176
Q

What cancer is there an increased risk of with primary sclerosing cholangitis

A

Cholangiocarcinoma

177
Q

What is an indication of acute liver failure on blood test

A

Raised INR

178
Q

Describe one of the liver signs for right sided heart failure

A

Firm, smooth, tender and pulsatile liver edge

179
Q

Drugs that cause Cholestasis

A

COCP
Abx: fluclox, co-amoxiclav, erythromycin
Anabolic steroids, testosterone
Phenothiazines
Sulphonylureas
Fibrates
Nifedipine

Junior Surgery (6 decks)

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