General Surgery Flashcards

1
Q

What clinical signs are consistent with Pancreatic Cancer?

A

Trousseau’s sign

Courvoisier’s sign

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2
Q

What is Courvoisier’s sign?

A

A painless palpable gallbladder

Jaundice

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3
Q

What is Trousseau’s sign?

A

Migrator thrombophlebitis

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4
Q

What is a Zenker’s diverticulum?

A

Pharyngeal pouch - small bump in the pharynx, most common in the elderly

It occurs through a weakness in the muscle layer called the Killian dehiscence

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5
Q

How does a pharyngeal pouch usually present?

A
Dysphagia 
Chronic cough 
Weight loss 
Regurgitation 
Aspiration
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6
Q

How is a pharyngeal pouch diagnosed?

A

Barium swallow

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7
Q

Following initial resuscitation what should be given to patients awaiting endoscopy after an oesophageal varicie bleed?

A

IV Abx

Terlipressin

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8
Q

How should a perinatal abscess be managed?

A

Incision and drainage

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9
Q

Features of Lynch syndrome?

A

Strong familial prevealence of colorectral, endometrial cancer and ovarian cancer

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10
Q

Best initital management for patients with output stomas?

A

Restrict oral hypotonic fluid intake
Advise dextrose-saline solution
Prescribe oral loperamide and omeprazole

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11
Q

What is offered at the age of 55 as part of the NHS screening programme for colorectal cancer?

A

One-off flexible sigmoidoscopy

Detect and remove polyps

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12
Q

What type of colorectal tumours are suitable for anterior resection?

A

Anterior resection for tumours >8 cm from the anal canal or involving the proximal 1/3 of the rectum.

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13
Q

What tumours are a left hemicolectomy suitable for?

A

A left hemicolectomy is suitable for tumours of the distal transverse colon and descending colon

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14
Q

What are the components of Dukes staging of colorectal canceR?

A

A: limited to the bowel wall (i.e. not beyond the muscularis).
B: extending through the bowel wall (i.e. beyond the muscularis).
C: regional lymph node involvement.
D: distant metastaseis.

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15
Q

What diagnostic investigation is most sensitive for a hiatal hernia?

A

Barium swallow

Will demonstrate if the stomach is partially or completely intrathroacic

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16
Q

What drugs commonly cause cholestasis?

A
Coamoxiclav 
Flucloxacillin
Nitrofurintonin 
Steroids 
Sulphonylurea
Prochlorperazine
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17
Q

How is bilirubin conjugated and excreted?

A

Bilirubin is conjugated with glucuronic acid by glucronyltransferase and is then excreted in the bile.
In the bowel, bilirubin is converted to stercobilin by gut flora, which is then excreted in the faeces as well as urobilinogen, which is reabsorbed and converted into bile, excreted in the faeces or excreted in the urine.

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18
Q

What cancer is most associated with Barrets oesophagus?

A

Oesophogeal adenocarcinoma

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19
Q

What type of calcium distrubance is most commonly associated with abdominal pain#?

A

Hypercalcemia

If calcium is low suspect acute pancreatitis

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20
Q

What drug is used for acute management of a variceal haemorrhage?

A

Terlipressin

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21
Q

How does a pharangeal pouch present?

A

Dysphagia
Aspirtation pneumonia
Halitosis

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22
Q

What is the most common kind of stomach ulcer?

A

Duodenal

Gastric are less common

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23
Q

What kind of stomach ulcers are more likely to have associated weight loss?

A

Gastric ulcers

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24
Q

What kind of stomach ulcers have epigastric pain worsened by eating?

A

Gastric ulcers

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25
Q

What type of ulcer may occur at a stoma sight?

A

Pyoderma gangrenosum, a deep, painful, ulcer

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26
Q

Initial management of acute limb ischemia?

A

Analgesia
IV heparin
Vascular review

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27
Q

Common conseuqence of terminal ileus resection

A

Bile acid malabsorption

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28
Q

What is Mirrizi’s syndrome?

A

Causes an obstructive jaundice due to compression of the common bile duct secondary to presence of gallstones in the cystic duct itself or in Harmanns pouch
Conjugated hyperbilirubinaemia
Diagnosis confirmed by MRCP
Management laproscopic cholecystectomy

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29
Q

Definitive diagnostic test for acute mesenteric ischemia?

A

CT angiography

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30
Q

What is meant by the acute abdomen?

A

Recent, rapid onset of urgent abdominal or pelvic pathology, usually presenting with abdominal pain

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31
Q

Causes of generalised abdominal pain?

A

Peritonitis
Ruptured AAA
Intestinal obstruction
Ischemic colitis

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32
Q

Causes of right upper quadrant pain?

A

Bilary colic
Acute cholecystitis
Acute cholangitis

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33
Q

Causes of epigastric pain?

A

Acute gastritis
Peptic ulcer disease
Pancreatitis
Ruptured AAA

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34
Q

Causes of central abdominal pain?

A

Ruptured AAA
Intestinal obstruction
Ischemic colitis
Early stage of appendicitis

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35
Q

Causes of RIF pain?

A
Acute appendicitis
Ectopic pregnancy
Ruptured ovarian cyst
Ovarian torsion
Meckel's diverticulitis
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36
Q

Causes of LIF pain?

A

Diverticulitis
Ectopic pregnancy
Ruptured ovarian cysts
Ovarian torsion

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37
Q

What is suprapubic pain?

A

Lower urinary tract infection
Acute urinary retention
PID
Prostatitis

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38
Q

Causes of loin to groin pain?

A

Renal colic (kidney stones)
Ruptured AAA
Pyelonephritis

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39
Q

Causes of testicular pain?

A

Testicular torsion

Epididymo-orchitis

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40
Q

What is peritonitis?

A

Inflammation of the peritoneum (lining of the abdomen)

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41
Q

Signs of peritonitis?

A

Guarding (involuntary tensing of the abdominal wall muscles when palpated to protect the painful area below)
Rigidity (involuntary persistent tightness of abdominal wall muscles)
Rebound tenderness (releasing pressure causes more pain than the pressure itself)
Coughing test (coughing results in pain)
Percussion tenderness
Reduced/absent bowel sounfs (suggestive of paralytic illeus)

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42
Q

What causes localised peritonitis?

A

Underlying organ inflammation

Appendicitis, cholecystitits

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43
Q

What causes generalised peritonitis?

A

Perforation of an abdominal viscous(e.g. perforated duodenal ulcers, ruptured appendix) releasing contents into the peritoneal cavity and causing generalised inflammation of the peritoneum

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44
Q

What causes spontaneous bacterial peritonitis?

A

Spontaneous infection of ascities in patients with liver disease. Treated with broad spectrum antibiotics, carries a poor prognosis

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45
Q

How might you investigate the acute abdomen?

A

FBB: hb, WBC
U&E - electrolyte imbalance, kidney functions, prior to CT
LFTs give and indication of the bilary and hepatic systems
CRP - gives an indication of inflammation and infection
Amyalse gives an indication of inflammation of the of the pancreas
INR - synthetic liver fucntion, plus prep for procedure
Serum calcium - scoring acute pancreatitits
Beta-HCG in females of child bearing age
ABG - lactate (ischema) and pO2 (acute pancreatitis scoring)
Group and save - may req blood transfusion
Abdominal x ray: can show evidence of bowel obstruction (dilated loops)
Erect CXR: air under diaphragm when intra-abdominal perforation (pneumoperitoneum, air in abdominal cavity)
Abdominal USS: gallstones, billary duct dilation, gynae pathology
CT scans: identify the cause of an acute abdomen and determine management
Urine dip: UTI, haematuria

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46
Q

Initital management of a bowel obstruction?

A
NBM
NG tube
IV fluids
Analgesia
Anit-emetics
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47
Q

Causes of acutte abdomen that could lead to hypovolemic shock?

A

AAA
Ruptured ectopic pregnancy
Bleeding gastric ulcer
Trauma

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48
Q

Signs of hypovolemic shock?

A
Tachycardia
Hypotension
Pale 
Clammy 
Cool to touch
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49
Q

What, until proven otherwise, should be suspected in a patient with severe abdominal pain out of proprotion to their clinic signs? What other signs might be present?

A

Ischemic bowl
Acidaemic
Raised lactate
Diffuse, constant pain

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50
Q

What is colic?

A

Abdominal the crescendos to become very severe and then completely goes away

  • billary
  • ureteric
  • bowel obstruction
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51
Q

What is peritonism?

A

Localised inflamation of the peritoneum, usually due to inflammation of a ciscus that then irritates the visceral (and subsequently, parietal peritoneum) before localising to another area or becoming generalised

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52
Q

What is looked for on USS KUB?

A

Hydronephrosis

Cortico-medullary differentiation

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53
Q

What is looked for in billary tree USS?

A

Presence of gallstones
Gallbladder thickening
Duct dilation

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54
Q

Why should patients with abdominal pain have an ECG?

A

Exclude cardiac pain (reffered)

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55
Q

Where do the vast majority of gastric cancers arise from?

A

Gastric mucosa (adenocarcinoma)

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56
Q

Adenocarcinoma makes up 90% of stomach cancers, what are the other types?

A

Conncective tissue, lymphoid or neuroendocrine mallignancy

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57
Q

Risk factors for gastric cancer?

A
H pylor infection
Male gender
INcreasing age
Smoking
Alcohol consumption 
High salt diet, positive family history, pernicious anaemia
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58
Q

What is H. Pylori?

A

H. Pylori is a gram negative helical bacterium that produces the urease enzyme
Breaks down urea into CO2 and ammonia
Ammonia neutralises stomach acid allowing the bacteria to to create an alkaline microenvironment

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59
Q

How does H pylori lead to gastric neoplasia?

A

Sets off a cycle of repeated damage to the epithelial cells, leading to inflammation, ulceration and ultimately gastric neoplasia.

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60
Q

What are the presenting symptoms of gastric cancer?

A
Dyspepsia (new onset, non-responsive to PPI)
Dysphagia
Early satiety
Vomiting 
Melena
Heametemisis
Constitutional symptoms (late stage)
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61
Q

How can H pylori be diagnosed?

A

Blood antigen test
Stool antigen test
Urea breath test

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62
Q

How is H pylori erradicated?

A

PPI
Clarithromycin
Amoxocillin

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63
Q

What clinical signs may be present in late stage gastric cancer?

A
Palpable epigastric mass
Troisier signs (palpable left supraclavicular (Virchow) node) in metastatic abdominal malignancy

Mets: Hepatomegaly, ascites, jaundice, acanthosis nigricans

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64
Q

Differentials for gastric cancer?

A

Peptic ulcer disease
GORD
Gallstone disease
Pancreatic cancer

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65
Q

How is suspected gastric cancer investigated?

A

FBC
LFTs
Upper GI endoscopy (OGD) +/- biopsy
CT chest-abdo-pelvis and staging laparoscopy (peritoneal mets) to stage

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66
Q

Why are PET scans rarely used in staging gastric cancers?

A

Gastric cancers to not take up the radioactive tracer well

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67
Q

How are gastric cancers staged?

A

TNM

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68
Q

What should biopsies from gastric mallignancies be sent for?

A

Histology - grading of any neoplasia
CLO test - H pylroi
HER2/neu protein expression - allows target monotherapies if present

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69
Q

What is the mainstay of curative treatment in gastric cancer?

A

Surgery (+ adjuvant and neoadjuvant chemotherapy if tolerated)
Proximal gastric cancer - total gastrectomy
Distal gastric cancer (antrum or pylorus) - subtotal gastrectomy

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70
Q

What may patients with early T1a gastric tumours be offered as an alternative to total or sub-total gastrectomy?

A

Endoscopic Mucosal Resection (EMR) is suitable for tumours confined to the muscularis mucosa and has reduced morbidity and mortality

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71
Q

What is the most commonly used method in reconstruction the alimentary anatomy following gastrectomy?

A

Roux-en-Y reconstruction (best functional result, less bile reflux)
Distal oeosphagus is end to end anatsomosed with the small bowel
Proximal small bowel is end- to - side anastamosed to the small bowel

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72
Q

Complications of gasterectomy?

A
Anastomotic leak 
Re-operation
Dumping syndrome 
Vitamin B-12 deficiency 
Death (3-5%)
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73
Q

What injection do patients require 3 monthly following gastrectomy?

A

Vitamin B12

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74
Q

What is the palliative management of gastric cancer?

A

Chemotherapy
Stention
Surgery (distal gastrectomy or bypass surgery, gastro-jejunostomy) if stenting fails or unavailable, or in palliation of bleeding gasrtic tumours
Best supportive care

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75
Q

Most common complications of gastric cancer?

A

Gastric outlet obstruction, iron-deficiency anaemia, perforation, malnutrition

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76
Q

What is gastric dumping syndrome?

A

Common following gastric bypass surgery
Early (10-30 mins post prandial) - Sudden and large passage of hypertonic gastric contents into the small intestine, resulting in an intraluminal fluid shift and subsequent intestinal distention
Late (1-3 hours post prandial) Surge in insulin production following the ‘dumping’ of food results in hypoglycemia

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77
Q

Presentation of gastric dumping syndrome~?

A

Early (10-30 mins post prandial): nausea, vommiting, diarrhoea, hypovolemia, leading to synpathetic response predominating with tachycardia and diaphoresis
Late (1-3 hours post prandial) - hypoglycemia

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78
Q

How can gastric dumping syndrome be managed?

A

Small volume and more frequent meals, avoidence of simple carbohydrates, separation of eating and drinking to reduce load on stomach.
Refer these patients to a dietician?
Treat hypoglycemia, intra-operative glucose management

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79
Q

Most common symptoms of dumping syndrome?

A
Sweating
Tingling lips or extremities
Tremor
Dizziness 
Slurred speech
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80
Q

When should a patient be referred under the urgent pathway for OGD?

A

New onset dysphagia or aged >55 years presenting with weight loss and either upper abdominal pain, reflux, or dyspepsia

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81
Q

What are the main two types of oesophageal cancer?

A

Squamous cell carcinoma (developing world)

Adenocarcinoma (developed world)

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82
Q

Where does SCC typically occur in the oesophagus?

A

Middle and upper thirds

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83
Q

What is oesophageal SCC associated with?

A
Smoking
Excessive alcohol consumption
Chronic achalasia
Low vitamin A levels
Iron def
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84
Q

What is oesophageal adneocarcinoma associated with?

A

Metaplastic epithelium - Barrett’s oesophagus (progressing to dysplasia)
GORD
Obesity
High fat intake

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85
Q

Where in the oesophagus does adenocarcinoma typically occur?

A

Lower thirds

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86
Q

What vasculature runs near the oesophagus?

A

Inferior thyroid artery
Azygous vein
Thoracic aorta and oesophogeal branches

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87
Q

How does oesophageal cancer present?

A

Late stage usually
Dysphagia, progressive, starting with solids progressing to liquids
Odynophagia
Hoarseness
Cachexia, dehydration
Supracavicular lymphandenopathy
Signs of metastatic disease: jaundice, heaptomgealy, asicities)

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88
Q

How is dysphagia investigated?

A

Upper GI endoscopy (OGD) within two weeks +/- biopsy for histology
CT chest-abdomen-pelvis if OGD abnormal to search for mets
PET-CT for “
Staging laparoscopy for junctional tumours with an intra-abdominal component to look for intra-peritoneal metasteses
FNA of any palpable cervical lymph nodes
Bronchoscopy if hoarseness or haemoptysis

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89
Q

How is oesophageal SCC managed?

A

Usually palliative

Curative: chemo-radiotherapy

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90
Q

How is oesophogeal adenocarcinoma managed?

A

Mostly palliatively, but if curative treatment:
Neo-adjuvant chemothreapy or chemo-radiotherapy followed by oesophageal resection (oesophagectomy or EMR if high grad Barret’s or early stage cancer)

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91
Q

Oesphagectomy involved removing the tumour, top of stomach and surrounding lymph nodes. The stomach is made into a conduit and borugh up the chest to replace the oesophagus. One lung needs to be deflated during surgery for aprox two hours, and patients will not recover fully for 6-9 months.
What surgical approaches may be taken?

A

Right thoracotomy with laparotomy - Ivor-Lewis procedure
Right thoracotomy with abdominal and neck incision - MecKeown procedure
Left thoracotomy with or without neck incision
Left thoraco-abdominal incision (starting above umbilicas extending round back to below left shoulder blade)

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92
Q

Palliative options for oesophogeal cancer?

A

Oesophageal stent
Radiotherapy and or chemotherapy can be used to reduce tumour size and bleeding
Nutritional support: thicken fluids, nutritional supplements, RIG if enteral feeds not tolerated

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93
Q

At what vertebral level does the oesophagus originate?

A

C6

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94
Q

Aetiology of acute pancreatitits?

A
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune (SLE, Sjorgen's)
Scorpion venom
Hypercalcemia
ERCP
Drugs
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95
Q

What drugs may cause acute pancreatitis?

A

Azathioprine
NSAIDs
Diuretics

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96
Q

How is acute pancreatitis distinguished from chronic pancreatitis?

A

Extent of damage to the secretory function of the gland - no gross structual damage in acute

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97
Q

Pathogenisis of acute pancreatitis?

A

Premature and exaggerated activation of digestive enzymes within the pancreas
Pancreatic inflammatory response causes and increase in vascular permeability
Subsequent fluid shifts (third spacing)
Enzymes released from pancreas into the systemic circultion
Autodigestion of fats and blood vessels (fat necrosis, bleeding into retroperitoneal space)
Release of free fatty acides reacts with serum calcium to cause chalky depsosits in the fatty tissue, resulting in hypocalcemia

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98
Q

What does severe end-stage pancreatitis result in?

A

Partial or complete necrosis of the pancreas

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99
Q

How does pancreaitits present?

A

Sudden onset of severe epigastric pain which can radiate through to the back
Nausea and vommiting
Epigastric tenderness +/- gaurding
Cullen’s sign, Grey turner’s sign
Tetany (from hypocalcemia)
Concurrent obstructive jaundice (if gallstone aeitiology)

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100
Q

WHat is Cullen’s sign?

A

Bruising around the umbilicus

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101
Q

What is Grey Turner’s sign?

A

Flank brusing

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102
Q

Why does Cullen’s and Grey Turner’s signs occur?

A

Retroperitoneal haemmorhage

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103
Q

Causes of abdominal pain radiating to the back?

A
Pancreatiitis (chronic or acute)
AAA
Renal calculi
Aortic dissection
Peptic ulcer disease
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104
Q

How should you investigate acute pancreatitis (excluding routine bloods as per abdominal pain)

A

Serum amylase
LFTs - concurrent cholestatic elemant to the clinical pictutre
Serum lipase
Abnominal USS - ?gallstone
Contract CT if USS inconclusive, and also 6-10 days after admission in patient with features of persistent inflammatory response or organ failure

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105
Q

Whilst not routinely performed for acute pancreatitis, an AXR can show what?

A

Sential loop sign - dilated proximal bowel loop adjacent to the pancreas, which occurs secondary to the localised inflammation

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106
Q

When should a CXR be performed in acute pancreatitits?

A

Look for pleural effusion or ARDS

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107
Q

What serum amylase is diagnostic of acute pancreatitits?

A

3x the upper limit of normal, although not related to disease severity

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108
Q

What ALT level strongly suggest gallstone ateiology in acute pancreatitits?

A

> 150

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109
Q

What is the most accurate blood test for acute pancreatitis and why is it not used?

A

Serum lipase
Remains elevated longer than amylase
Not available our routinely performed in many hospitals

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110
Q

What is used to asses the severity of acute pancreatitits within the first 48 hours of admission?

A

Modified glasgow criteria

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111
Q

What is the modified Glasgow criteria?

A
pO2 <8kPa
Age > 55
Neutrophiles (WCC>15)
Calcium <2
Renal (urea>16)
Enzymes LDH>600 or AST>200
Albumin <32
Sugar > 10
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112
Q

What does it mean if a patient has 3 or more factors within the first 48 hours of admission of the modified Glasgow criteria?

A

Severe pancreatitis, high dependency care referral warrented

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113
Q

What will a contrast-enhanced CT scan show after 48hr of initial presentation of acute pancreaitits?

A

Pancreatic odema and swelling

Non-enhancing areas suggestive of pancreatic necrosis

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114
Q

How is acute pancreatitits managed?

A

IV fluid resucitation - balanced crystalloid
O2 as required
NG tube if vomiting profusely
Catheterisation to monitor urine out put (aim >0.5ml/kg/hr)
Opiod analgesia

If gallstones ERCP and spinchterotomy

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115
Q

When should a borad-spectrum antibiotic such as imipenem be considered for prophalaxis against infection in acute pancreatitits?

A

confirmed pancreatic necrosis

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116
Q

What should be advised once a patient with pancreatitis secondary to gallstones has been stablised?

A

Early laparoscopic cholecystectomy

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117
Q

What complications of pancreatitis tend to occur within days of initial onset?

A
Systemic complications such as:
Disseminated Intravascular Coagulation DIC
Acute Respiratory Distress Syndrome
Hypocalcemia
Hyperglycemia
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118
Q

Why might hyperglycemia occur secondary to pancreatitits?

A

Destruction of islets of Langerhans and subesquent disturbances to insulin metabolism

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119
Q

What should be suspected in patients with evidence of persistent systemic inflammation for more than 7-10 days after the onset of pancreatitis?

A

Ischemic infarction of the pancreatic tissue, confirmed by CT imaging

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120
Q

How is pancreatic necrosis managed?

A
Pancreatic necrosectomy (open or endoscopic)
Broad spectrum abx
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121
Q

Definitive diagnosis of infected pancreatic necrosis can be confirmed by what?

A

FNA

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122
Q

What is a pancreatic pseudocyst?

A

Collection of fluid containing pancreatic enzymes, blood and necrotic tissue, can occur anywhere within or adjacent to the pancreas
Lack an epithelial lining, instead have a vascular and fiboritic wall surrounding the collection

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123
Q

Where to pancreatic pseudocysts typically occur?

A

Lesser sac obstructing the gastro-epiploic foramen by inflammatory adhesions

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124
Q

How long after the initial acute pancreatitis episode do pancreatic pseudocyts tend to occur?

A

Weeks

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125
Q

How are pancreatic pseudocyts managed?

A

About 50% will spontaneously resolve, hence conservative management is usually the initial treatment of choice. Cysts which have been present for longer than 6 weeks are unlikely to resolve spontaneously. Treatment options include surgical debridement or endoscopic drainage
N.B. prone to haemorrhage or rupture, can become infected

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126
Q

What is a stoma?

A

Surgically created opening into a hollow organ

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127
Q

What does a colonostomy open into?

A

Large bowel

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128
Q

What does an ileostomy open into?

A

The ileum

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129
Q

What does a urostomy open into?

A

The urinary system

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130
Q

What are colostomy stomas situated?

A

Left illiac fossa

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131
Q

Where are ileostomys siutated?

A

Right iliac fossa

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132
Q

What stomas will be spouted?

A

Ileostomy

Urostomy

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133
Q

What stoma is flush to the skin?

A

Colonoscopy

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134
Q

What with the conistency of an ileostomy be?

A

Watery, greener

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135
Q

What is to consistency of a colonostomy contents?

A

Thick and sludgey

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136
Q

What will urostomy output look like?

A

Urine

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137
Q

How many lumens does a loop stoma have?

A

Two

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138
Q

How many lumens does an end stoma have?

A

One

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139
Q

Potential complications of a stoma?

A
Parastomal hernia (colostomy)
Prolapse
Retraction
Infarction (turns jet black)
Ulceration
Fistulation
Local skin irritation 
Loss of bowel length leading to high output dehydration and malnurtition 
Granulomas causing raised red lumps around the stoma 
Stenosis 
Constipation (colostomies)
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140
Q

Where are urostomies usually located?

A

RIF

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141
Q

What is an end colostomy?

A

Removal of a section of bowel, where the end part of the proximal bowel is brough onto the skin. The other open end of remaining bowel (distal part) is sutured and left in the abdomen. It may be reversed at a later date, were the two ends are sutured together, creatining an anastomisis

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142
Q

When are end colostomies permanent?

A

End colostomies are permanent after resection of abdomino-perineal resection (APR) because the entire rectum and anus have been removed. These are usually located in the lower left abdomen.

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143
Q

What procedure forms an end illeostomy?

A

Panproctocolectomy
End ileostomies are permanent after a panproctocolectomy (total colectomy with removal of the large bowel, rectum and anus)

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144
Q

What is a panproctocolectomy?

A

Total collectomy with removal of the large bowel, rectum and anus

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145
Q

What is a panproctocolectomy used to treat?

A

IBD

Familial adenmoatous polyposis (FAP)

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146
Q

Alternative to panproctocolectomy?

A

Ileo-anal anastomosis (J-pouch)

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147
Q

What does a loop colostomy/ileostomy allow?

A

Distal portion of the bowel and anastomosis to heal after the surgery, allow faeces to bypass the distal, healing portion of the bowel until healed and ready to restart normal function, they are usually reveresed 6-8 hours.
The bowel is partially opened and folder so that there are two opening on the skin side-by-side, attached in the middle.
Proximal end is turned outside to form a spout, distal and is flatter.

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148
Q

How is a urostomy formed?

A

Creation of an ileal conduit.
Section of illeum removed and end-to-end anastomisis is screated so bowel in coninous. Ends of ureters are anatsomosed and separated to section the ileum. The end of the section is brough out onto the skin as a stoma and drains directly from the ureters into a urostomy bag.

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149
Q

What do gallstones form from?

A

Concentrated bile in the bile duct, most are made from cholesterol

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150
Q

Complications of gallstones?

A

Acute cholecystitits
Acute cholangitis
Pancreatitis (if blocking the pancreatic duct)
Obstructive jaundice

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151
Q

Basic anatomy of the bile duct system

A

Right and left hepatic ducts leave the liver and join together to become the common hepatic duct.
Cystic duct from gallbladder joins the common hepatic duct halfway along.
Pancreatic duct from the pancreas joints with the common hepatic duct further along.
Common bile duct and pancreatic duct join to become the ampulla of Vater, which opens into the duodenum.

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152
Q

What is the sphincter of Oddi?

A

Ring of muscle surrounding the ampulla of Vater that controls the flow of bile and pancreatic secretions in the duodenum.

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153
Q

What is cholestasis?

A

Blockage to flow of bile

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154
Q

What is cholelithiasis?

A

Presence of gallstones

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155
Q

What is choledocholithiasis?

A

Gallstones in the bile duct

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156
Q

What is billary colic

A

intermittent right upper quadrant pain caused by gallstones irritating bile ducts

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157
Q

What is cholecystitits?

A

Inflammation of the gallbladder

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158
Q

What is cholangitis?

A

Inflammation of the bile ducts

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159
Q

What is gallbladder empyema?

A

Pus in the gallbladder

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160
Q

What is a cholecystostomy?

A

Insertion of a drain into the gallbladder

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161
Q

What are the risk factors for gallstones?

A

Fat
Fair
Female
Forty

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162
Q

Typical presentation of gallstones (if symptomatic)

A

Billary colic
Severe, colicky epigastric or right upper quadrant pain
Often triggered by meals (particularly high fat meals)
Lasting between 30 minutes and 8 hours
May be associated with nausea and vomiting

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163
Q

What does raised jaundice, raised serum bilirubin, pale stools and dark urine represent?

A

Obstruction caused by a gallstone in the bile duct or an external mass pressing on the bile ducts (e.g. cholangiocarcinoma or tumour of head of pancreas)

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164
Q

What can a raised ALP indicated?

A
Liver pathology
Bone pathology (Paget's, bone malignancy)
Pregnancy (production by the placenta)
Billary obstruction 
Billary chirrosis
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165
Q

What are ALT and AST helpful markers of?

A

Hepatocellular injury

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166
Q

What does a higher ALP compared to AST and ALT?

A

Obstructive picture

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167
Q

What do a higher ALT and AST compared to ALP indicate?

A

Hepatic picture

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168
Q

First line investigation for suspected gallstone disease?

A

USS

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169
Q

What is USS of the bilary tract limited by?

A

Patient weight
Gaseous bowel obstructing the view
Discomfort from the probe

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170
Q

What might be found on USS of the billary tract?

A

Gallstones in the gallbladder
Gallstones in the ducts
Bile duct dilatation (normally less than 6mm diameter)
Acute cholecystitis (thickened gallbladder wall, stones or sludge in gallbladder and fluid around the gallbladder)
The pancreas and pancreatic duct

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171
Q

What is a magnetic resonance cholangio-pancreatography?

A

MRI scan with a specific protocol that produces a detailed image of the biliary system. It is very sensitive and specific for biliary tree disease, such as stones in the bile duct and malignancy.

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172
Q

When does gallstone disease warrent MRCP?

A

If USS does not show stones in the duct but there is bile duct dilation or raised bilirubin suggestive of obstruction

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173
Q

Key complications of ERCP

A

Excessive bleeding
Cholangitis (infection in the bile ducts)
Pancreatitis

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174
Q

The main indication for ERCP

A

Clear stones in the bile duct

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175
Q

What can be done during an ERCP?

A

Inject contrast and take x-rays to visualise the biliary system and diagnose pathology (e.g., stones or strictures)
Perform a sphincterotomy on the sphincter of Oddi if it is dysfunctional (blocking flow)
Clear stones from the ducts
Insert stents to improve bile duct drainage (e.g., with strictures or tumours)
Take biopsies of tumours

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176
Q

Complications of cholecystectomy?

A

Bleeding, infection, pain and scars
Damage to the bile duct including leakage and strictures
Stones left in the bile duct
Damage to the bowel, blood vessels or other organs
Anaesthetic risks
Venous thromboembolism (deep vein thrombosis or pulmonary embolism)
Post-cholecystectomy syndrome

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177
Q

What are the to approaches to cholecystectomy?

A

Laparoscopic

Open - Kocher incision

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178
Q

What is post-choecystectomy syndrome?

A
Diarrhoea
Indigestion
Epigastric or right upper quadrant pain and discomfort
Nausea
Intolerance of fatty foods
Flatulence
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179
Q

Why does post-cholecystectomy syndrome?

A

Attributed to changes in the bile flow after removal of the gallbladder

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180
Q

What is cutaneous wound healing?

A

Process by which the skin repairs itself after damage?

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181
Q

Types of wound healing?

A

Primary intention

Secondary intention

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182
Q

What are the four stages that occur in wound healing?

A

Haemostasis
Inflammation
Proliferation
Remoddeling

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183
Q

What happens in the hameostasis phase of primary intention

A

Action of platelets and cytokines forms a haematoma and
Causes vasconstriction, limiting blood loss at the affected area
The close proximity of the wound edges allows for ease of clot formation and prevents infection by forming a scab

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184
Q

What happens in the proliferation phase of primary intention healing?

A

Cytokines released by inflammatory cells drive the proliferation of fibroblasts
And formation of granulation tissue
Angiogenesis is promoted by the presence of growth mediators (e.g. VEGF)
Allows for further maturation of the granulation tissue
Production of collagen by fibroblasts
Allows for closure of wound within about a week

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185
Q

What happens in the inflammation phase of primary intention?

A

A cellular inflammation response acts to remove any cell debris and pathogens present

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186
Q

What is the remodelling phase of healing by primary intention?

A

Collagen fibres are deposited within the wound to provide strength in the region, with fibroblasts subsequently undergoing apoptosis

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187
Q

What is typically the end result of healing by primary intention?

A

Completed return to function with mininmal scaring and loss of skin appendages

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188
Q

Why is correct suture tension important?

A

Too loose and the wound edges will not be properly opposed, limiting the primary intention healing and reducing the wound strength
Too tight and the blood supply to the region may become compromised and lead to tissue necrosis and wound breakdown

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189
Q

What happens during haemostasis in secondary intention healing?

A

A large fibrin mesh forms which fills the wound

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190
Q

What happens in the inflammation phase of secondary intention?

A

An inflammatory response acts to remove and cell debris and pathogen present
Larger amount of cell debris present, and the inflammatory reaction tends to be more intense than in primary intention

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191
Q

What happens in the proliferation phase of secondary intention and why is it an important step?

A

Granulation tissue forms at the bottom of the wound
Important as the epithelia can only proliferate and regenerate once granulation tissue fills the wound to the level of the original epithelium, once the granulation tissue reaches this level the epithelia can completely cover the wound

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192
Q

What happens in the remoddeling stage of secondar intention healing?

A

Inflammatory response resolves, wound contraction occurs

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193
Q

When does healing by primary intention occur?

A

Wounds with dermal edges that are close together

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194
Q

When does healing occur by secondary intention?

A

When the sides of the wound are not opposed, therefore healing must occur from the bottom of the wound upwards?

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195
Q

What cells are vital in secondary intention?

A

Myofibroblasts - modified smooth muscle cells, that contain actin and myosin, and act to contract the wound; decreasing the space between the dermal edges. They also can deposit collage for scar healing.

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196
Q

What are keloid scars?

A

An uncommon complication from wound healing (particularly in people with darker skin) whereby there is excessive collage production, leading to extensive scarring. This can occur in both primary and secondary intention healing.

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197
Q

Local factors that affect wound healing?

A
Type, size, location of wound
Local blood supply
Infection
Foreign material or contamination
Radiation damage
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198
Q

What systemic factors affect wound healing?

A

Increasing age
Co-morbidities, especially CV disease or DM
Nutritional deficiencies (especially vitamin C)
Obestity

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199
Q

Four classes of surgical contamination?

A

Clean
Clean-contaminated
Contaminated
Dirty

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200
Q

What is clean contamination?

A

Elective, non-emergency, non-traumatic, and primary closed, with GI, biliary and GU tracts remaining intact

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201
Q

What is clean contamination?

A

Urgent or emergency case that is otherwise clean
Elective opening of respiratory tract, GI, bililary or GU tract with minimal spillage and not encountering infected urine or bile

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202
Q

What does contaminated mean?

A

Gross spillage from GI tract or entry into biliary or GU tract (in presence of infected bile or urine)
Penetrating trauma < 4 hours old or a chronic open wound to be grafted or covered

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203
Q

What is a dirty wound?

A

Purulent inflammation

Preoperative perforation of respiratory, GI, biliary, or GU tract, or a penetration trauma >4 hours old

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204
Q

Basic principals of management of a wound or laceration?

A
Haemostasis
Cleaning the wound
Analgesia
Skin closure
Dressing and follow-up advise
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205
Q

Methods to aid haemostasis?

A

Pressure
Elevation
Torniquet
Suturing

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206
Q

The five aspects of wound cleaning?

A

Disinfect - antiseptic
Decontaminate - removal forigen bodies
Debride devitalised tissue
Irrigate with saline (low perrsure as long as no obvious contamination)
Antibiotics for high risk wounds or signs of infection

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207
Q

Whats the maximum level of lidocan alone?

A

3mg/kg

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208
Q

Whats tha maximum level of lidocane with the addition of adrenaline?

A

7mg/kg

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209
Q

What’s the maximum level of lidocaine with the addition of adrenaline?

A

7mg/kg

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210
Q

When should adrenaline not be used with local anaesthetic?

A

If administering in or near appendages (e.g. a finger)

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211
Q

Methods of skin closure (manually opposed)?

A

Skin adhesive strips (if no risk factors for infection present)
Tissue adhesive glue (small laccerations with easily opposable edges)
Sutures (laceration greater than 5cm, deep dermal wounds, locations prone to flexion tension or wetting)
Staples (scalp wounds)

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212
Q

What should patients be advised following initial wound management?

A

Following initial wound management, advise patients to:

Seek medical attention for any signs of infection
Take simple analgesia (e.g. paracetamol)
Keep the wound dry as much as possible, even if wearing a waterproof dressing

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213
Q

How do you dress a wound to a non-infected laceration?

A

When applying a wound dressing to a non-infected laceration, the first layer should be non-adherent (such as a saline-soaked gauze), followed by an absorbent material to attract any wound exudate, and finally soft gauze tape to secure the dressing in place.

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214
Q

When should sutures or adhesive strips?

A

10-14 days after initial wound closure (or 3-5 days if on the head)

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215
Q

After how long will tissue adhesive flue naturally slough off?

A

1-2 weeks

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216
Q

Why do malnourished patients make poor surgical candiates?

A

Surgery causes physiological stress with a resultant hyper-metabolic state and catabolic response.
Malnourished patients have reduced nutritional reserves

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217
Q

How is BMI calculated?

A

Weight / Height2

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218
Q

What should be done with a patient with a MUST score of 1 (medium risk)

A

Document dietary intake for 3 days
If adequete repeat screening (hospital weekly, care home monthly, community 2-3monthly)
If inadequete clinical concern follow local policy

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219
Q

What should be done about a MUST score of 2 or more?

A

Dietician ref
Sets goals to improve and increase overall nutritional intake
Monitor and review care plan (weekly if in hospital otherwise monthly)

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220
Q

What BMI scores on a MUST calculation?

A

18.5-20 = 1

Under 18.5 = 2

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221
Q

What unplanned weight loss across 3-6 months scores on MUST?

A

5-10% = 1

Over 10 % = 2

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222
Q

What will be added to a patients MUST score if they are acutely ill and there has been or is likely to be no nutritional intake for >5 days?

A

2 points

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223
Q

Hiearchy of Feeding?

A
Oral nutritional supplements
NGT
PEG/RIG
Jeujunostomy
Paraentral nutrition
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224
Q

When should oral nutritional supplements be introduced?

A

If unable to eat sufficient calories

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225
Q

What should NGT feeding be used?

A

If unable to intake sufficient calories orally or dysfunctional swallow

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226
Q

When should gastostomy feeding (PEG/RIG) be used?

A

If oesophagus blocked/dysfunctional

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227
Q

When should jejunal feeding be used?

A

If stomach inaccessible or outflow obstruction

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228
Q

When should parentral nutrition be used?

A

If jejunum inaccessible or intestinal failure

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229
Q

What is the snap pneumonic for management of intestinal failure undergoing surgery?

A

Sepsis – Any overwhelming infection present must be corrected otherwise feeding will be largely useless
Nutrition – Once the infection is corrected, suitable nutritional support should be provided
Anatomy – Define the anatomy of the GI tract so that surgery can be planned
Procedure – Definitive surgery once any infection eradicated, the patient nourished, and the anatomy defined

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230
Q

What does a low serum albumin reflect?

A

A low serum albumin reflects either chronic inflammation, protein losing enteropathy, proteinuria, or hepatic dysfunction, but does not reflect malnutrition (as witnessed by the fact that patients with severe anorexia nervosa have a normal serum albumin).

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231
Q

Up to what point pre surgery can patients have clear fluids?

A

2 hours

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232
Q

From what period before surgery must a patient be NBM (excluding clear fluids)?

A

6 hours

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233
Q

Why should paients with entero-cutaneous fistulae avoid PN straight away ?

A

The proportion of ECF that will heal with PN is small.

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234
Q

How should patients with an entero-cutaneous fistula have their nutrition managed?

A
High fistula (jejunal): enteral or parentral nutrition
Low fistula (ileum/colon): treated with low fibre diet
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235
Q

How is a high output stoma managed?

A

Reduction in hypotonic fluids to 500ml/day
Reduction in gut motility with high dose loperamide and codeine phosphate
Reduction in secretions with high dose PPI BD
Use of WHO solution to reduce sodium losses
Low fibre diet to reduce intraluminal retention of water

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236
Q

Complications of TPN

A
Catheter placement and maintenance:
Pneumothorax
Thromboembolisim
Infections
IV nutrition
Fluid balance
Hyperglycemia/Hypoglycemia
Electrolyte imbalance (K, Phosp, Mg)
Hepatic toxicity
Bleeding
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237
Q

What is a fistula?

A

An abnormal connection between two epithelial surfaces

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238
Q

What does Hartmann’s procedure involve?

A

Removal of the rectosigmoid colon with closure of the anorectal stump and formation of a colostomy

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239
Q

What does Whipple’s procedure involve?

A

Removal of: Head of pancreas, duodenum, gallbladder, bile duct

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240
Q

What incision is used for renal transplant?

A

Hockey-stick incision

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241
Q

What might cause haematemisis?

A
Bleeding from part of the upper GI tract:
Oesophageal Varicies
Gastric ulceration
Mallor-Weiss Tear
Oesophagitis
Gastritis
Gastric mallginancy
Meckel's diverticulum
Dieulafoy lesions (vascular lesion)
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242
Q

Key facts to ascertain from a history and examination of upper Gi bleed?

A

Timing, frequency, volume of bleeding
History of dyspepsia, dysphagia or odynophagia
PMH and smoking and alcohol status
Steroids, NSAIDs, anticoagulants or bisphosphonates
Peritonism
Epigastric tendernies
Varacies of liver stigmata

243
Q

What are oeasophageal varacies?

A

Dilations of the porto-systemic venous anastomses in the oesophagus.
Dilated veins are swollen, thin-walled, and pront to rupture with the potential to cause a catastrophic haemmorhage
Most commonly caused by portal HTN secondary to alcoholic liver disease

244
Q

Where do gastric ulcers most commonly errode into the blood vessels supplying the upper GI tract?

A

Lesser curve of the stomach

Posterior duodenum

245
Q

What is a Mallory-Weiss tear?

A

Typified by episodes of severe or recurrent vomiting, then followed by haematemesis.
Forceful vomiting causes a tear in the epithelial lining of the oseophagus resulting in a small bleed
Benign

246
Q

What is oesophagitis?

A

Inflammation of the intraluminal epithelial layer of the oesophagus, most often due to gastric acid reflux or infections (Candida Albicans), medication (bisphosphonates), radiotherapy, injegstions of toxic substances or Crohn’s disease

247
Q

How should and upper GI bleed be investigated?

A

FBC (low Hb, although may not show intitially in an acute bleed)
U&Es (drop in urea:creatinine ratio very indicative of upper GI bleed)
LFTs (?liver damage cause)
Clotting
VBG/ABG - pH, base excess, lactate, signs of tissue hypoperfusion
Group and save (+cross match if suspected variceal bleed)
OGD is the definitive investigation and can form management
erect CXR if suspected peptic ulcer (pneumoperitoneum)
GT abdo with IV contrast (triple phase) assesing active bleeding if endoscopy unremarkable/too invasive

248
Q

What scoring system is used to risk stratify patients admitted with an upper GI bleed?

A

Glasgow-Blatchford score

249
Q

What score is used to asses the severity of GI bleeding post endoscopy?

A

Rockall

250
Q

What Glasgow-Blatchford score is associated with a >50% risk of needing intervention?

A

Greater than or equal to 6

251
Q

Definitive management of perforated peptic ulcer after initial resusitation?

A

Injections of adrenaline and cauterisation of the bleeding. High dose intravenous PPI therapy should be administered (e.g. IV 40mg omeprazole) to reduce acid secretion +/- H. Pylori eradication therapy if necessary

252
Q

Definitive management of oesophageal alongside initial resusitation and prophylactic abx?

A
Endoscopic banding
Somatostatin analogues (octreotide) or vasopressers (terlipressin) acting to reduce splanchic blood flow
253
Q

Long term management of oesophageal varicies?

A

Repeated banding

Beta-blocker therapy

254
Q

What is a Sengstaken-Blakemore tube and when is it used?

A

In severe oesophageal varices, inserted to level or varacies and inflated to compress the bleeding

255
Q

What is the most common artery affected by erosion due to a peptic ulcer?

A

This is most commonly the gastro-duodenal artery which is eroded into by an ulcer at the back of the first part of the duodenum.

256
Q

What plain film radiographic sign may indicate a perforated gastric ulcer?

A

Subdiaphragmatic free gas - suggest pneumoperitoneum

257
Q

How might an upper GI bleed present?

A

Haematemesis (vomiting blood)
“Coffee ground” vomit. This is caused by vomiting digested blood that looks like coffee grounds.
Melaena, which is tar like, black, greasy and offensive stools caused by digested blood
Haemodynamic instability occurs in large blood loss, causing a low blood pressure, tachycardia and other signs of shock. Bear in mind that young, fit patients may compensate well until they have lost a lot of blood.

258
Q

What does the Glasgow-Blatchford score take into account?

A
Drop in Hb
Rise in urea
Blood pressure
Heart rate
Melaena
Syncopy
259
Q

What does a Glasgow-Blatchford score of more than 0 indicate?

A

High risk for upper GI bleed

260
Q

What factors does the Rockall score take into account?

A

Age
Features of shock (e.g. tachycardia or hypotension)
Co-morbidities
Cause of bleeding (e.g. Mallory-Weiss tear or malignancy)
Endoscopic stigmata of recent haemorrhage such as clots or visible bleeding vessels

261
Q

Management of an upper GI bleed (ABATED)

A

A – ABCDE approach to immediate resuscitation
B – Bloods
A – Access (ideally 2 large bore cannula)
T – Transfuse
E – Endoscopy (arrange urgent endoscopy within 24 hours)
D – Drugs (stop anticoagulants and NSAIDs)

262
Q

What do NICE reccomend regarding PPIs in relation to OGD for oesophageal varicies?

A

Against PPI prior to endoscopy

263
Q

What causes melena to be tarry, offensive smelling and difficult to flush away?

A

Alteration and degration of blood by intestinal enzymes

264
Q

Most common causes of melena?

A
Peptic ulcer disease
Variceal bleeds
Upper GI mallignancy (ulcerating oesophageal or gastric malignancies)
Mallory-Weiss tear
Meckel's diverticulum
Vascular malformations
265
Q

When should peptic ulcer disease be suspected as the cause of an Upper GI Bleed?

A

Known active peptic ulcer disease
History of NSAIDs or steroid use
Previous dyspepsia-like symptoms
H.pylori positive

266
Q

When does the most significant bleeding occur in gastric ulcer disease?

A

When the ulcer erodes through the posterior gastric wall into the gastroduodenal artery

267
Q

What examination must be performed to confirm melena?

A

DRE

268
Q

Management of bleeding peptic ulcer?

A

Adrenaline injections
Cauterisation of bleeding
High dose PPI (e.g. IV 4omg omperazole)

269
Q

Below what Hb should blood products be transfused?

A

<70g/L or <80 if hx of CVD

270
Q

Why is a rise in the urea:creatinine ratio an indicator of an upper GI bleed?

A

Digested blood produces urea as a by-product

271
Q

What is haematochezia?

A

Passage of fresh blood PR

272
Q

Causes of rectal bleeding?

A
Diverticular disease
Ischemic of infective collitis
Haemorrhoids
Mallignancy
Angiodysplasia
Crohn's disease
UC
Radiation proctitis
Large upper GI bleed
273
Q

What are diverticula?

A

Outpouchings of the bowel wall composed only of muscosa

274
Q

Where are diverticula most commonly found?

A

Descending sigmoid colon

275
Q

Diverticular disease bleeds vs diverticulitis associated bleeds?

A

Diverticular disease - painless

Diverticulitis - painful (secondary to localised inflammation)

276
Q

What are haemorrhoids?

A

Pathogically engorged vascular cusions in the anal canal

277
Q

How might haemorrhoids present?

A

PR mass
Pruritis
Fresh red rectal bleed, on toilet pan or stool surface
Painful if large haemorrhoids thrombose

278
Q

In patients with PR bleeding, what key aspects should be ascertained from history and examination?

A

Nature of bleeding, including duration, frequency, colour of the bleeding, relation to stool and defecation
Associated symptoms, including pain (especially association with defaecation), haematemesis, PR mucus, or previous episodes
Family history of bowel cancer or inflammatory bowel disease
Localised tenderness in the abdomen
Abdominal mass palpable
DRE - assess for rectal masses and ongoing presence of blood

279
Q

What score is used to help stratify patients presenting with a lower GI bleed to determine if outpatient management is feasible?

A

Oakland score

280
Q

What factors determine Oakland score?

A
Age
Sex
Previous admissions for lowe GI bleed
PR findings
HR
Systolic BP
Hb
281
Q

What investigations should be performed on stable patients with rectal bleeding?

A

FBC
LFT
Clotting
U&Es
?Stool culture
Flexible sigmoidoscopy or colonoscopy (if inconclusive) to exclude left-colonic pathology (outpatient)
If no abnormality identified on flexi sig or colonoscopy - OGD
If OGD also inconclusive: capsule endoscopy, MRI small bowel

282
Q

Risk factors of adverese outcomes from acute rectal bleeding?

A
Haemodynamic instability
Ongoing haematochezia
Age > 60
Serum creatnine >150umol/L
Significant co-morbidities
283
Q

What investigations should be performed on unstable patients with rectal bleeding?

A
FBC
LFT
Clotting
U&Es
?Stool culture
Urgent CT angiogram to find ource of bleeding (+/- theraputic intervention:emoblisation)
284
Q

How are PR bleeds managed if unstable?

A

IV fluids and blood transfusion of packed RBC as required
Urgent reversal of anticoagulants
Endoscopic haemostasis methods
Arterial embolisation (patients with an identified bleeding point (blush) of sufficient size on angiogram

285
Q

What are possible methods of endoscopic haemostasis?

A

Injection (diluted adrenaline)
Contact and non contact thermal devices (bipolar electrocoagulation or argon plasma coagulation)
Mechanical therapies (endoscopic clips and band ligation)

286
Q

What is the blood supply to the ileum?

A

Superior mesenteric artery

287
Q

Which value in clotting screen is most affected by warfarin?

A

Prothrombin time

288
Q

What is diverticulosis

A

The presence of diverticula (asymptomatic, incidental on imaging)

289
Q

What is diverticular disease/diverticulosis?

A

Symptoms arising from diverticula

290
Q

What is diverticulitis?

A

Inflammation of the diverticula

291
Q

What is a diverticular bleed?

A

The diverticulum erodes into a vessel and causes a large volume painless bleed

292
Q

What is a diverticular abscess?

A

A diverticular abscess (often termed a pericolic abscess) occurs as a sequelae in complicated diverticulitis

Those that are around <5cm can generally be managed with conservatively with intravenous antibiotics, as this is effective in ~90% of cases. If the abscess is any bigger, then radiological drainage is first-line treatment.

Complicated multi-loculated abscesses (or patients who clinically deteriorate) will need surgical intervention, either with a laparoscopic washout or a Hartmann’s procedure.

293
Q

Investigation of choice for suspected diverticulitis?

A

CT abdo pelvis

294
Q

Indications for surgical intervention in diverticulitis?

A

Intestinal bleeding
Failure of percutaneous drainage
Septic shock

295
Q

How can 1st and second degree haemorrhoids be managed if symptomatic?

A

Rubber band ligation

296
Q

Why are external haemorrhoids painful (unlike internal)?

A

They are below the dentate line/pectinate line
Superior to the pectinate line – visceral innervation is from the inferior hypogastric plexus.
Inferior to the pectinate line – somatic innervation derived from the inferior anal (rectal) nerves, branches of the pudendal nerve. This part of the anal canal is sensitive to pain, touch, and temperature

297
Q

Conservative management of haemorrhoids?

A

Increase dietary fiber
Increase fluid intake
Laxatives if necessary
Topical analgesia (lignocaine gel)

298
Q

What is haemorrhoidal artery ligation suitable for?

A

2nd or 3rd degree haemorrhoids

299
Q

What is Haemorrhoidectomy suitable for?

A

3rd degree and 4th degree haemorrhoids

300
Q

Describe 1st degree haemorrhoids?

A

Remain in the rectum

301
Q

Describe 2nd degree haemorrhoids?

A

Prolapse through the anus on defecation but spontaneously reduce

302
Q

Describe 3rd degree haemorrhoids?

A

Prolapse through the anus on defecation but require digital reduction

303
Q

Describe 4th degree haemorrhoids?

A

Remain persistently prolapsed

304
Q

What is Charcot’s triad and when does it appear?

A

Right upper quadrant pain
Fever
Jaundice (raised bilirubin)

Acute cholangitis

305
Q

How and why will excessive vommiting affect pH?

A

Vomiting leads to the loss of the hydrogen ions secreted by the stomach. Hydrogen ions are needed to create acidity within the body, so a loss of these ions will lead to alkalosis. This results in metabolic alkalosis.

306
Q

Why do direct inguinal hernias occur?

A

Direct inguinal hernias occur due to weakness in the abdominal wall at Hesselbach’s triangle.

307
Q

What is an indirect inguinal hernia?

A

An indirect inguinal hernia is where the bowel herniates through the inguinal canal.

308
Q

What is the inguinal canal

A

The inguinal canal is a tube that runs between the deep inguinal ring (where it connects to the peritoneal cavity), and the superficial inguinal ring (where it connects to the scrotum). In males, the inguinal canal is what allows the spermatic cord and its contents to travel from inside the peritoneal cavity, through the abdominal wall and into the scrotum.

309
Q

How, on examination, can you differentiate between a direct and indirect inguinal hernia?

A

When an indirect hernia is reduced and pressure is applied (with two fingertips) to the deep inguinal ring (at the mid-way point from the ASIS to the pubic tubercle), the hernia will remain reduced.

310
Q

Where is the deep inguinal ring?

A

The mid-way point from the ASIS to the pubic tubercle

311
Q

What do femoral hernias involve?

A

Femoral hernias involve herniation of the abdominal contents through the femoral canal. This occurs below the inguinal ligament, at the top of the thigh.

312
Q

What are obturator hernias?

A

Obturator hernias are where the abdominal or pelvic contents herniate through the obturator foramen at the bottom of the pelvis.

313
Q

Where does a spigelian hernia occur?

A

A Spigelian hernia occurs between the lateral border of the rectus abdominis muscle and the linea semilunaris. This is the site of the spigelian fascia, which is an aponeurosis between the muscles of the abdominal wall.

314
Q

What is paralytic illeus?

A

Condition affecting the small bowel, where the normal peristalsis that pushes the contents along the length of the intestines, temporarily stops

315
Q

What causes paralytic illeus?

A

Injury to the bowel
Handling of the bowel during surgery (most common)
Inflammation or infection in, or nearby, the bowel (e.g., peritonitis, appendicitis, pancreatitis or pneumonia)
Electrolyte imbalance (e.g., hypokalaemia or hyponatraemia)

316
Q

Why is biliary colic particularly associated with fatty meals?

A

Meals high in fat stimulate the release of cholecystokinin (CCK) from the duodenum. This peptide hormone stimulates the contraction of the muscles of the gallbladder. When the gallbladder is full of stones, this causes pain as the gallbladder contracts against the stones.

317
Q

What is Rovsing’s sign?

A

In acute appendicitis, palpation of the left iliac fossa causes pain in the RIF

318
Q

Where will be particularly tender in the abdomen in acute appendicitis?

A

McBurney’s point

319
Q

Where is McBurney’s point?

A

A specific area one-third of the distance from the anterior superior iliac spine (ASIS) to the umbilicus.

320
Q

What is tenesmus?

A

Tenesmus: the sensation of needing to open bowels without being able to produce stools (often accompanied by pain)

321
Q

What does a sigmoid volvulus show on XR?

A

Coffee bean sign

322
Q

What surgical procedure can be used to manage sigmoid volvulus?

A

Hartman’s

323
Q

Which anti-emetics are suitable in bowel obstruction secondary to mechanical obstruction and which are not?

A

Prokinetic antiemetics such as metoclopramide should be avoided in a bowel obstruction secondary to a mechanical obstruction, as they stimulate peristalsis. Cyclizine would be an appropriate choice of antiemetic.

324
Q

Risk factors for acute mesenteric ischemia?

A
Female
Older age
AF
HTN
Hypercholestrolaemia
325
Q

What ABG abnormalities may be present in acute mesenteric ischemia?

A

High lactate

Metabolic acidosis

326
Q

What is the gold standard for diagnosis of acute mesenteric ischemia?

A

Contrast CT scan

327
Q

Contraindications to liver transplant?

A

Significant co-morbidities (e.g., severe kidney, lung or heart disease)
Current illicit drug use
Continuing alcohol misuse (generally 6 months of abstinence is required)
Untreated HIV
Current or previous cancer (except certain liver cancers)

328
Q

Causes of microcytic anaemia?

A
T – Thalassaemia
A – Anaemia of chronic disease
I – Iron deficiency anaemia
L – Lead poisoning
S – Sideroblastic anaemia
329
Q

What is Courvoisier’s law and what does it suggest?

A

Courvoisier’s law states that a palpable gallbladder along with jaundice is unlikely to be gallstones. The cause is usually cholangiocarcinoma or pancreatic cancer.

330
Q

What is the most applicable tumour marker for bowel cancer?

A

Serum carcinoembryonic antigen (CEA)

331
Q

What is Carbohydrate antigen 19-9 (CA 19-9) most associated with?

A

Pancreatic cancer and colangiocarcinoma?

332
Q

What is a Meckel’s diverticulum?

A

Meckel’s diverticulum is a malformation of the distal ileum that occurs in around 2% of the population. It is usually asymptomatic and does not require any treatment. However, it can bleed, become inflamed, rupture or cause a volvulus or intussusception. An inflamed Meckel’s diverticulum (Meckel’s diverticulitis) may mimic the presentation of appendicitis.

333
Q

What Gi cancer is alfapetoprotein associated with?

A

Liver

334
Q

What is sigmoid volvulus?

A

Sigmoid volvulus is more common than caecal volvulus and tends to affect older patients. The twist affects the sigmoid colon. A key cause is chronic constipation and lengthening of the mesentery attached to the sigmoid colon. The sigmoid colon becomes overloaded with faeces, causing it to sink downwards, resulting in a twist. It is also associated with a high fibre diet and the excessive use of laxatives. Neuropsychiatric disorders (e.g., Parkinson’s) and being a nursing home resident are also risk factors.

335
Q

What is the preferred management of rectal tumours over 8 cm from the anal margin?

A

Anterior resection

336
Q

What does anterior resection involve?

A

Removal of diseased segment, formation of a primary anastomosis between the remaining proximal colon and distal rectum. Temporary loop ileostomy is typically performed to allow the distal anastomoses to heal.

337
Q

What is the preferred management of rectal tumours less than 8 cm from the anal margin?

A

Abdomino-perianal resection with temporary loop ileostomy

338
Q

What does AP resection involve?

A

Removal of anus, rectum and proximal sigmoid colon through both abdominal and perineal acesss
The remaining section of the colon is brought out to the surface in a permanent end colostomy

339
Q

If a patient has a colostomy and no anus what procedure are they likely to have?

A

AP resection

340
Q

If a patient has a colostomy and an anus what procedure are they likely to have?

A

Emergency Hartmann’s procedure

341
Q

Where might an epigastric hernia be found and what causes them?

A

Protusion of extra-peritoneal fat or omentum through a defect in the linea alba vetween the xiphisternum and umbilicus

342
Q

How are epigastric hernias managed?

A

Asymptomatic: address risk factors such as obesity

Symptomatic or cosmetic concerns: Surgical repair

343
Q

What level of rapid unintentional weight loss is suspicious for mallignancy?

A

> 5%

344
Q

Which cancer is most strongly associated with a history of primary sclerosing cholangitis?

A

Cholangiocarcinoma

345
Q

What side is colonic cancer most common on?

A

Left-sided colonic cancer

346
Q

Why is right sided colon cancer more likely to be severe?

A

Later presentation, insidious in nature

347
Q

Why does right sided colon cancer rarely cause obstructive symptoms?

A

Stool in right sided colon is semi-liquid

348
Q

What is the treatment for Plummer Vinson what triad of symptoms does it present with?

A

Iron def anaemia
Glossitis
Dysphagia

Endoscopy shows oesophageal webs
Treated with iron supplements and mechanical dilation of the oesophagous

349
Q

What does an enlarged Virchow’s node suggest?

A

GI malignancy

350
Q

What is Virchow’s node?

A

Left supraclavicular lymph node

351
Q

What is a hernia?

A

Weak point in a cavity wall (usually muscle or fascia) which allows a body organ normally contained within that cavity to pass through that cavity wall

352
Q

Typical features of abdominal wall hernias?

A

A soft lump protruding from the abdominal wall
The lump may be reducible (it can be pushed back into the normal place)
The lump may protrude on coughing (raising intra-abdominal pressure) or standing (pulled out by gravity)
Aching, pulling or dragging sensation

353
Q

What are the three key complications of a hernia?

A

Incarceration
Obstruction
Strangulation

354
Q

What is meant by incarceration of a hernia?

A

The hernia cannot be reduced back to its proper position (it is irreducible)
Bowel is trapped in the herniated position
(may lead to obstruction or strangulation)

355
Q

What is meant by obstruction of a hernia?

A

Causes blockage in the passage of feaces through the bowel.

Obstruction presents with vomiting, generalised abdominal pain and absolute constipation

356
Q

What is strangulation of a hernia?

A

Hernia is NON-REDUCIBLE and the base of the hernia become so tight that it cuts off the blood supply leading to ISCHEMIA

357
Q

What makes a hernia at lower risk of complication?

A

Size of neck/defect - wide neck - less complications

358
Q

How will strangulation of a hernia present?

A

Significant pain and tenderness at hernia site

Clinical features of mechanical obstruction: absolute constipation, N&V

359
Q

Why is hernia strangulation a surgical emergency?

A

Bowel will die (infarct) within hours if not corrected surgically

360
Q

What is a Richter’s hernia?

A

A Richter’s hernia is a very specific situation that can occur in any abdominal hernia. This is where only part of the bowel wall and lumen herniate through the defect, with the other side of that section of the bowel remaining within the peritoneal cavity. They can become strangulated, where the blood supply to that portion of the bowel wall is constricted and cut off. Strangulated Richter’s hernias will progress very rapidly to ischaemia and necrosis and should be operated on immediately.

361
Q

What is a Maydl’s hernia?

A

Maydl’s hernia refers to a specific situation where two different loops of bowel are contained within the hernia.

362
Q

General management options of all abdominal hernias?

A
Conservative management (wide neck hernias)
Tension free repair - mesh over the defect in the abdominal wall is sutured into the muscles and tissues on the other side of the defect, covering it and preventing herniation. Tissues eventually grow over the mesh and provide extra support.
Tensions repair: suturing of the muscles and tissues on either side of the defect back together - pain and high recurrence - rarely used
363
Q

Advantages and disadvantages of tension-free hernia repair?

A

Lower recurrence rate compared with tension repair, but there may be complications associated with the mesh (e.g., chronic pain).

364
Q

Diferntials for a lump in the inguinal region?

A
Indirect or direct inguinal hernia
Femoral hernia
Lymph node
Saphena varix
Femoral aneurysm
Abscess
Undecended/ectopic testes
Kidney transpant
365
Q

What is saphena varix and what might it be mistaken as?

A

DIlation of saphenous vein at junction with femoral vein in groin
Inguinal hernia

366
Q

What anatomical abnormality can lead to indirect inguinal hernias?

A

After embryological development, in some patients, the inguinal ring remains patent, and the processus vaginalis remains intact. This leaves a tract or tunnel from the abdominal contents, through the inguinal canal and into the scrotum. The bowel can herniate along this tract, creating an indirect inguinal hernia.

367
Q

What are the borders of Hesselbach’s triangle?

A
Rectus abdominis muscle - medial boarder
Inferior epigastric vessels - superior/lateral border
Pouparts ligament (inguinal ligament) inferior border
368
Q

Relationship of a direct inguinal hernia to the inferior epigastric vessels?

A

Direct inguinal hernias protrude anteromedial and inferior to the course of the inferior epigastric vessels

369
Q

Relationship of an indirect inguinal hernia to the inferior epigastric vessels?

A

Indirect inguinal hernias protrude posterolateral and superior to the course of the inferior epigastric vessels

370
Q

Why should femoral hernias be managed surgically, ideally within two weeks of presentation?

A

High risk of strangulation as femoral ring leaves only a narrow opening

371
Q

Where do femoral hernias occur?

A

(Potrusion of abdominal contents through the femoral ring) below the inguinal ligament at the top of the thigh

372
Q

What are the boundaries of the femoral canal?

A

Femoral vein - laterally
Lacunar ligament medially
Inguinal ligament posteriorly
Pectineal ligament posteriorly

373
Q

What are incisional hernias, when do they occur and how are the managed?

A

Incisional hernias occur at the site of an incision from previous surgery. They are due to weakness where the muscles and tissues were closed after a surgical incision. The bigger the incision, the higher the risk of a hernia forming. Medical co-morbidities put patients at higher risk due to poor healing.

Incisional hernias can be difficult to repair, with a high rate of recurrence. They are often left alone if they are large, with a wide neck and low risk of complications, particularly in patients with multiple co-morbidities.

374
Q

In which patients do umbilical hernias tend to occur in?

A

Neonates (usually resolve spontaneously)
Older people
due to a defect in the muscle around the umbilicus

375
Q

What is the spigelian fascia?

A

Aponeurosis between the muscles of the abdominal wallk

376
Q

How can diagnosis of a spiglian hernia be established?

A

USS

377
Q

What kind of base to spigelian hernias tend to have?

A

Narrow base, increased risk of complications

378
Q

Why does anastomotic leak cause fever?

A

Free fluid causes irritation of the peritoneum

379
Q

What is diastasis recti?

A

Widening of the linea alba, forming a larger gap between the rectus muscles.
It is not technically a hernia.
Gap becomes most prominent when the patient lies on their back and lifts their head
There is a protuding buldge along the middle of the abdomen
Congenital, pregnancy, obesity
Normally no treatment but surgical repair is possible

380
Q

What is an obturator hernia?

A

Abdominal or pelvic contents herniate through the obturator foramen at the bottom of the pelvis, due to a defect in the pelvice floor.
More common in older women who have had pregnancies and vaginal deliveries.

381
Q

Obturator hernias are usually asymptomatic, if they do have symptoms, what might they be?

A

Irritation to the obturator nerve, causing pain in the groin or medial thigh

382
Q

What is the Howship-Romberg sign?

A

Pain extending to the inner thigh to the knee when the hip is internally rotated due to compression of the obturator nerve

383
Q

What are the four types of hiatus hernia?

A

Type 1 - Sliding
Type 2 - Rolling
Type 3 - combination of sliding an rolling
Type 4 - large opening with additional abdominal organs entering the thorax (e.g. bowel, pancreas, omentum)

384
Q

What is a hiatus hernia?

A

An hiatus hernia refers to the herniation of the stomach up through the diaphragm. The diaphragm opening should be at the level of the lower oesophageal sphincter and should be fixed in place. A narrow opening helps to maintain the sphincter and stop acid and stomach contents refluxing into the oesophagus. When the opening of the diaphragm is wider, the stomach can enter through the diaphragm and the contents of the stomach can reflux into the oesophagus.

385
Q

What is a sliding hiatus hernia?

A

Stomach slides up through the diaphragm with the gastro-oesophageal junction passing up into the thorax

386
Q

What is a rolling hiatus hernia?

A

Seperate portion of the stomach (ie. fundus) folds around and enters through the diaphragm opening, alongside the oesophagus

387
Q

How might a hiatus hernia present?

A
Dyspepsia 
Heartburn 
Acid reflux
Reflux of food
Burping
Bloating
Halitosis (bad breath)
388
Q

Why might hiatus hernias not be picked up by investigation’?

A

They can be intermittent

389
Q

How can hiatus hernias be investigated?

A

Chest c ray
CT scan
Endoscopy
Barium swallow testing

390
Q

How are hiatus hernias treated?

A

Conservative (with GORD treatment)

Surgical repair if high risk of complications or symptoms are resitant to medical treatment

391
Q

How is hiatus hernia manage surgically?

A

Laparoscopic fundoplication - fundus of the stomach around the lower oesophagus to narrow the lower oesophageal sphincter

392
Q

What is a bowel obstruction?

A

A bowel obstruction refers to when the passage of food, fluids and gas, through the intestines becomes blocked. Small bowel obstruction is more common than large bowel obstruction. Obstruction results in a build up of gas and faecal matter proximal to the obstruction (before the obstruction). This causes back-pressure, resulting in vomiting and dilatation of the intestines proximal to the obstruction. Bowel obstruction is a surgical emergency.

393
Q

What is third-spacing?

A

Fluid loss from the intravascular space into the gastrointestinal tract. Less bowel over which fluid can be reabsorbed.
Leads to hypovalemia and shock

394
Q

Causes of small bowel obstruction?

A

Adhesions (small bowel)
Hernias (small bowel)
Malignancy (large bowel)

395
Q

Causes of large bowel obstruction?

A

Volvulus (large bowel)
Diverticular disease
Strictures (e.g., secondary to Crohn’s disease)
Intussusception (in young children aged 6 months to 2 years)

396
Q

Main causes of intestinal adhesions?

A

Abdominal or pelvic surgery (especially open)
Peritonitis
Adominal or pelvic infections (e.g. PID)
Endometriosis

397
Q

What is meant by closed loop obstruction?

A

Two points of obstruction along the bowel

398
Q

What might cause a closed loop obstruction?

A
  1. Adhesions that compress two areas of bowel
  2. Hernias that isolate a section of bowel blocking either end
  3. Volvulus where the twist isolates a section of intestine
  4. A single point of obstruction in the large bowel, with an ileocaecal valve that is competent
399
Q

Why does a competent ilecaecal valve cause problems?

A

A competent ileocaecal valve does not allow any movement back into the illeum from the caecum.
LBO and competent ileocacel valve, a section of bowel becomes isolated and the contents cannot flow in either direction

400
Q

Why does a close-loop obstruction of the bowel require emergency surgery?

A

Contents of obstruction cannot do not have an open end where they can drain and decompress.
Therefore, the closed loop section will inevitably continue to expand, leading to ischemia and perforation.

401
Q

Key features of bowel obstruction?

A

Vomiting (particularly green bilious vomiting) - earlier in SOB
Abdominal distention
Diffuse abdominal pain
Absolute constipation and lack of flatulence
“Tinkling” bowel sounds may be heard in early bowel obstruction

402
Q

Upper limits of the normal diameter of bowel?

A

The upper limits of the normal diameter of bowel are:

3 cm small bowel
6 cm colon
9 cm caecum

403
Q

Key finding on abdominal x ray of bowel obstruction?

A

Distended bowel loops

404
Q

Investigation of choice for chronic bowel ischemia? What will it demonstrate?

A

Mesenteric angiography

Demonstrate a proximal occlusion of mesenteric vessels or vasoconstriction of all the mesenteric arcades

405
Q

How does chronic pancreatitis typically present?

A

Epigastric pain that radiates through the back (exaccerbated by fatty food or alcohol, relieved by sitting forwards)
Steratohorea
Weight loss
Diabetes melitus (Polydyspia, polyuria)

406
Q

What is Borhaave’s syndrome?

A

Oesophageal rupture secondary to forceful vomiting
Triad of: Vomiting, chest pain and subcutaneous emphysema

(Epigastric back pain may occur)

407
Q

What HPB complication might co-amoxiclav cause?

A

Cholestatic jaundice

408
Q

How will small bowel vs large bowel appear on X ray?

A

Small bowel: 3cm, vavulae conniventes (muscosal folds) for lines extending the full width of the bowel. Central
Large bowel: 6cm (9cm ceacam), hasutra (pouches formed by muscle wall) extending partial width of the bowel, peripheral

409
Q

Reasons why a patient with a bowel obstruction may be haemodynamically unstable?

A

Hypovolaemic shock due to fluid stuck in the bowel rather than the intravascular space (third-spacing)
Bowel ischaemia
Bowel perforation
Sepsis

410
Q

Key blood test findings in bowel obstruction?

A

U&Es- electrolyte imbalance

VBG - Metabolic alkalosis, raised lactate (bowel ischemia)

411
Q

Initial management of bowel obstruction?

A

NBM
IV fluids to hydrate and correct electrolyte imbalances
NG tube insertion with free drainage, reduces risk of vomiting and apsiration
Anti-emetics if NG aspirate minimal -NOT metoclopramide

412
Q

Initital imaging for bowel obstruction?

A

Abdominal X ray
OR CT scan if signs and symptoms are clear
CXR demonstrates air under diagphragm if intra-abdominal perforation
Contrast CT to confirm diagnosis, site and cause of obstruction. Also diagnose any intra-abdominal perforation

413
Q

Indications for surgical intervention in bowel obstruction?

A
Failed conservative managemet after 48hrs 
Closed loop bowel obstruction
Strangulater hernia, obstruction tumour
Intestinal obstruction
Virgin abdomen (never had surgery)
414
Q

Complications of bowel obstruction?

A

Bowel ischaemia
Bowel perforation leading to faecal peritonitis (high mortality)
Dehydration and renal impairment

415
Q

What should be done when a SBO is not resolving within 24 hours of conservative treatment?

A

A water soluble contrast study should be performed in cases that do not resolve within 24 hours conservative management. If contrast does not reach the colon by 6 hours then it is very unlikely that it will resolve and the patient should be taken to theatre.

416
Q

What are the surgical options in treating bowel obstruction?

A

Laparoscopy or lapaotomy to correct underlying cause
Emergency resection of the obstruction tumour
Adhesiolysis
Hernia repair
Explorative surgery if unclear cause
During colonoscopy stent can be inserted if obstruction due to tumour

417
Q

What is appendicitis and when is the peak incidence?

A

Inflammation of the appendix (small, thin tube arising from the caecum, with a single dead end opening to the bowel)
10 - 20 years
(second smaller peak around 60-70)

418
Q

What is the pathophysiology of acute appendicitis?

A

Pathogens get trapped due to obstruction at the point where the appendix meets the bowel (where the three teniae coli meet)
Trapping of pathogens leads to inflammation
Inflammation may proceed to gangrene and rupture
When the appendix ruptures, faecal contents and infective material are released into the peritoneal cavity, leading to peritonitits, which is inflammation of the peritoneal lining

419
Q

Signs and symptoms of appendicitis?

A
Central abdominal pain that localised to RIF within 24 hrs
Tenderness at McBurney's point (refers to a specific are one third of the distance from the ASIS to the umbilicus)
Anorexia
N&V
Low grade fever
Rovsings signs
(Psoas sign)
Guarding on abdominal palpation
Rebound tenderness in the RIF
Percussion tenderness
420
Q

What findings upon abdominal examintation suggest peritonitis?

A

Rebound tenderness

Percussion tenderness

421
Q

How is appendicitis diagnosed?

A
Usually only:
Raised inflammatory markers
Clinical presentation
Diagnostic laparoscopy + appendectomy (if indicated)
Diagnosis can be further confirmed by:
USS to exclude ovarian pathology
CT scan confirms appendicitis
422
Q

Key differential diagnoses of appendicitis?

A

Ectopic pregnancy
Ovarian cyst rupture/torsion
Meckel’s Diverticulum
Mesenteric adenitits

423
Q

What is mesenteric adenitis?

A

Mesenteric adenitis describes inflamed abdominal lymph nodes. It presents with abdominal pain, usually in younger children, and is often associated with tonsillitis or an upper respiratory tract infection. No specific treatment is required.

424
Q

What is Meckel’s diverticulum?

A

Meckel’s diverticulum is a malformation of the distal ileum that occurs in around 2% of the population. It is usually asymptomatic and does not require any treatment. However, it can bleed, become inflamed, rupture or cause a volvulus or intussusception.

425
Q

What is an appendix mass and how is it managed?

A

Mass occuring when the omentum surrounds and sticks to the inflamed appendix, forming a mass in the RIF
Managed conservatively with supportive treatment and abx, then once condition has resolved definitive appendectomy.

426
Q

Complications of Appendicetomy?

A
Bleeding, infection, pain and scars
Damage to bowel, bladder or other organs
Removal of a normal appendix
Anaesthetic risks
Venous thromboembolism (deep vein thrombosis or pulmonary embolism)
427
Q

What is a volvulus?

A

Condition where bowel twists itself around the mesentery that it is attatched too

428
Q

What is meant by bowel mesentery?

A

Membranous potential tissue that creates a conncetion between the bowel and the posterior abdominal wall, through which the mesenteric arteries supply blood to the bowel

429
Q

What kind of bowel obstruction does a vovulus?

A

Close loop large bowel obstruction

430
Q

How can volvulus cause bowel ischemia and what can this cause?

A

Blood vessels that supply the bowel can be involved, cutting off the blood supply to the bowel, which leads to bowel ischemia, which can lead to necrosis and bowel perforation

431
Q

What type of volvulus is most common?

A

Sigmoid volvulus

432
Q

What kind of volvulus affects older patients?

A

Sigmoid volvulus

433
Q

Key cause of sigmoid volvulus and pathophysiology?

A

Chronic constipation and lengthening of the mesentery attatched to the sigmoid colon.
Sigmoid colon becomes overloaded with faeces, causing it to sink downwards causing a twist.
It is also associated with a high fibre diet and the excessive use of laxatives

434
Q

Which type of volvulus tends to affect younger patients?

A

Caecal volvulus

435
Q

Risk factors of volvulus?

A
Neuropsychiatric disorders (e.g., Parkinson’s)
Nursing home residents
Chronic constipation
High fibre diet
Pregnancy
Adhesions
436
Q

Investigation of choice to confirm volvulus and identify other pathology?

A

A contrast CT scan

437
Q

How is caecal volvulus managed surgically?

A

Ileocaecal resection or right hemicolectomy for caecal volvulus

438
Q

How is sigmoid volvulus managed surgically?

A

Hartmann’s procedure

439
Q

Which surgical option can be used to manage any kind of volvulus?

A

Laparotomy

440
Q

Conservative management of sigmoid volvulus?

A

Conservative management with endoscopic decompression can be attempted in patients with sigmoid volvulus (without peritonitis)
A flexible sigmoidoscope is inserted with the patient lying in the left lateral position, correcting the volvulus, a flatus tube is left in place (decompress) and later removed

441
Q

What sign may be present on CT IV contrast in a volvulus?

A

The whirlpool sign of the mesentery, also known as the whirl sign, is seen when the bowel rotates around its mesentery leading to whirls of the mesenteric vessels

442
Q

Disadvanatge to conservate management of volvulus?

A

High risk of recurrence

443
Q

How do diverticula form?

A

Circular muscle in LI is penetrated at points by blood vessels - area of weakness
INcreased pressure inside the lumin over time causes a gap to form in these areas of circular muscle
These gaps allow muscose to herniate through the muscle layer and pouches to form diverticula

444
Q

Why do divertiucula nor form in the rectum?

A

It has outer longitudinal muscle layer completely surrounding its diameter adding extra support

445
Q

Which areas of colon are susseptible to formation of diverticula?

A

Areas not covered by tenia coli (strips formed by three longitudinal muscles running along the colon)

446
Q

Most uncommon type of diverticula?

A

Small bowel

Sigmoid most common

447
Q

Risk factors for diverticulosis?

A

Increased age (wear and tare)
Low fiber diet
Obesity
Use of NSAIDs (increases risk of diverticular haemorrhage)

448
Q

How is diverticulosis found incidently?

A

Colonoscopy or CT

449
Q

How should asymptomatic diverticula be managed?

A

High fiber diet and weight loss if appropriate

450
Q

If diverticulosis causes LIF pain, constipation, or rectal bleeding, how is it managed?

A
  1. Bulk forming laxatives (ispaghula husk, methylcellulose)
    2, Increased fibre intake
  2. AVOID stimulant laxatives such as Senna
  3. If symptoms are significant and persistant, surgery to remove affected area
451
Q

How might acute diverticulitis present?

A

Pain and tenderness in the left iliac fossa / lower left abdomen
Fever
Diarrhoea
Nausea and vomiting
Rectal bleeding
Palpable abdominal mass (if an abscess has formed)
Raised inflammatory markers (e.g., CRP) and white blood cells

452
Q

How is uncomplicated diverticulitis managed in primary care?

A

Oral co-amoxiclav (at least 5 days)
Analgesia (avoiding NSAIDs and opiates, if possible)
Only taking clear liquids (avoiding solid food) until symptoms improve (usually 2-3 days)
Follow-up within 2 days to review symptoms

453
Q

How is diverticulitis with severe pain or complications, warrenting hospital admission, treated?

A
NBM/clear fluids only
IV abx
IV fluids
Analgesia
Urgent investigation - CT
Urgent surgery to treat complications as required
454
Q

What are the potential complications of acute diverticulitis?

A

Perforation
Peritonitis
Peridiverticular abscess
Large haemorrhage requiring blood transfusions
Fistula (e.g., between the colon and the bladder or vagina)
Ileus / obstruction

455
Q

What three main branches of the abdominal aorta supply the abdominal organs?

A

Coeliac artery
Superior mesenteric artery
INferior mesnetric artery

456
Q

Which section of gut does the coeliac artery supply?

A

Foregut
Distal end of the esophagus, the stomach, and a first half of the descending portion of the duodenum, biliary system, liver, pancreas, spleen

457
Q

What section of gut does the superior mesenteric artery supply?

A

Midgut - distal part of the duodenum to first part of transverse colon

458
Q

What section of gut does the inferior mesenteric artery supply?

A

Hind gut - second half of transverse colon to the rectum

459
Q

What is chronic mesenteric ischemia also known as?

A

Intestinal angina

460
Q

What does chronic mesenteric ischemia result from?

A

Narrowing of the mesenteric blood vessels by atherosclerosis

461
Q

What is the main presenting feature of chronic mesnteric ischemia?

A

Intermittent abdominal pain, when the blood supply cannot keep up with the demand

462
Q

Triad of symptoms in chronic mesenteric ischemia?

A
Central colicky abdominal pain after eating (starting around 30 minutes after eating and lasting 1-2 hours)
Weight loss (due to food avoidance, as this causes pain)
Abdominal bruit may be heard on auscultation
463
Q

Risk factors for chronic mesenteric ischemia?

A
Increased age
Family history
Smoking
Diabetes
Hypertension
Raised cholesterol
464
Q

Management of chronic mesenteric ischemia?

A

Reduce modifiable risk factors
Secondary CVD prevention - statins, antiplatelet medication
Revascularisation to improve blood flow to the intestines

465
Q

How can revascularisation be performed in chronic mesenteric ischemia?

A

Endovascular procedures - first line (Percutaneous mesenteric artery stenting)
Open surgery - second line (endarectomy, re-implantation, bypass grafting)

466
Q

What causes acute mesenteric ischemia?

A

Acute mesenteric ischaemia is typically caused by a rapid blockage in blood flow through the superior mesenteric artery. This is usually caused by a thrombus (blood clot) stuck in the artery, blocking blood flow. The blood clot may be a thrombus that has developed inside the artery or an embolus from another site that has got stuck in the artery.

467
Q

Which condition is a key risk factor for acute mesenteric ischemia and why?

A

AF
Thrombus forms in left atrium, thromboembolises down the aorta to the superior mesenteric artery where it becomes stuck and cuts of the blood supply

468
Q

How does acute mesenteric ischemia present?

A

acute, non-specific abdominal pain. The pain is disproportionate to the examination findings

469
Q

The mortality of acute mesenteric ischemia is over 50%, what potential complications can arise from it??

A
Shock
Peritonitis
Sepsis
Bowel ischemia leading to necrosis leading to perforation 
Metabolic acidosis 
Raised lactate
470
Q

What abnormality will be present on VBG in a patient with acute mesenteric ischemia?

A

Metabolic acidosis with raised anion gap

Raised lactate

471
Q

Goal of surgical management in acute mesenteric ischemia?

A

Remove necrotic bowel

Remove or bypass the thrombus in the blood vessel (open surgery or endovascular procedures may be used)

472
Q

Risk factors for bowel cancer?

A

Family history of bowel cancer
Familial adenomatous polyposis (FAP)
Hereditary nonpolyposis colorectal cancer (HNPCC), also known as Lynch syndrome
Inflammatory bowel disease (Crohn’s or ulcerative colitis)
Increased age
Diet (high in red and processed meat and low in fibre)
Obesity and sedentary lifestyle
Smoking
Alcohol

473
Q

What is familial adenomatous polyposis (FAP)?

A

Autosomal dominant condition
Malfunctioning of tumour superssion genes (adenomatous polyposis coli - APC)
Polyps - adenomas - develop along large intestine, have potential to become cancerous (before pt is 40)
Pt advised to undergo prophylactic panproctocolectomy

474
Q

What is Lynch syndrome?

A

Hereditary nonpolyposis colorectal cancer (HNPCC) is also known as Lynch syndrome.
It is an autosomal dominant condition
Results from mutations in DNA mismatch repair (MMR) genes.
Patients are at a higher risk of a number of cancers, but particularly colorectal cancer.
Unlikely FAP, it does not cause adenomas and tumours develop in isolation.

475
Q

Red flags for bowel cancer?

A

Change in bowel habit (usually to more loose and frequent stools)
Unexplained weight loss
Rectal bleeding
Unexplained abdominal pain
Iron deficiency anaemia (microcytic anaemia with low ferritin)
Abdominal or rectal mass on examination

476
Q

What is the criteria for bowel cancer two week wait referral in a patient over 40 years?

A

Abdominal pain and unexplained weight loss

477
Q

What is the criteria for bowel cancer two week wait referral in a patient over 50 years?

A

Unexplained rectal bleeding

478
Q

What is the criteria for bowel cancer two week wait referral in a patient over 60?

A

Change in bowel habit or iron def anaemia

479
Q

What screening test is used to look for bowel cancer and who is it offered to?

A

In England, people aged 60 – 74 years are sent a home FIT test to do every 2 years. If the results come back positive they are sent for a colonoscopy.
People over 50 with unexplained weight loss and no other symptoms who do not meet 2ww criteria
Under 60s with a change in bowel habit who do not meet criteria for 2ww

480
Q

Who is offered colonscopy at regular intervals without a FIT test?

A

Patients with risk factors such as
FAP
HNPCC
IBD

481
Q

What do Faecal immunochemical tests look for specifically?

A

Human haemoglobin in the stool

482
Q

Gold standard investigation for bowel cancer?

A

Colonoscopy +/- biopsy or tattoo suspicious lesion

483
Q

What is sigmoidoscopy, what is it used for and what is the weakness of using it?

A

Sigmoidoscopy involves an endoscopy of the rectum and sigmoid colon only. This may be used in cases where the only feature is rectal bleeding. There is the obvious risk of missing cancers in other parts of the colon.

484
Q

What may be used in diagnosis of bowel cancer in patients not fit for colonoscopy?

A

CT colonography is a CT scan with bowel prep and contrast to visualise the colon in more detail. This may be considered in patients less fit for a colonoscopy but it is less detailed and does not allow for a biopsy.

485
Q

What is used when investigating staging in a patient with bowel cancer?

A

Staging CT scan involves a full CT thorax, abdomen and pelvis (CT TAP). This is used to look for metastasis and other cancers. It may be used after a diagnosis of colorectal cancer, or as part of the initial workup in patients with vague symptoms (e.g., weight loss) in addition to colonoscopy as an initial investigation to exclude other cancers.

486
Q

What tumour marker can be used in prediciting relapse in patinets previously treated for bowel cancer?

A

Carcinoembryonic antigen (CEA)

487
Q

What is, from A-D Duke’s classification of bowel cancer?

A

Dukes A – confined to mucosa and part of the muscle of the bowel wall
Dukes B – extending through the muscle of the bowel wall
Dukes C – lymph node involvement
Dukes D – metastatic disease

488
Q

What classification has replaced Dukes’ classification of bowel cancer?

A

TMN classification

489
Q

T of TNM?

A

TX – unable to assess size
T1 – submucosa involvement
T2 – involvement of muscularis propria (muscle layer)
T3 – involvement of the subserosa and serosa (outer layer), but not through the serosa
T4 – spread through the serosa (4a) reaching other tissues or organs (4b)

490
Q

N of TNM?

A

NX – unable to assess nodes
N0 – no nodal spread
N1 – spread to 1-3 nodes
N2 – spread to more than 3 nodes

491
Q

N of TNM?

A

NX – unable to assess nodes
N0 – no nodal spread
N1 – spread to 1-3 nodes
N2 – spread to more than 3 nodes

492
Q

M of TMN?

A

M0 – no metastasis

M1 – metastasis

493
Q

Factors MDT will consider when managing colorectal cancer?

A
Clinical condition
General health
Stage
Histology
Patient wishes
494
Q

Management of bowel cancer?

A

Surgical resection
Chemotherapy
Radiotherapy
Palliative care

495
Q

What does, generally, surgical management of bowel cancer involve?

A

Identifying the tumour (it may have been tattooed during an endoscopy)
Removing the section of bowel containing the tumour,
Creating an end-to-end anastomosis (sewing the remaining ends back together)
Alternatively creating a stoma (bringing the open section of bowel onto the skin)

496
Q

What is removed in a right hemicolectomy?

A

Caecum
Ascending
Proximal transverse colon

497
Q

What does a left hemicolectomy involve removing?

A

Distal transverse and descending colon

498
Q

What is removed and what is psared in a low anterior resection?

A

Removal of sigmoid colon and upper rectum

Sparing of the lower rectum and anus

499
Q

What does a high anterior resection involve removal of?

A

Sigmoid colon (including anus and all of the rectum)

500
Q

What does an abdomino-perineal resection inolve?

A

Involves removing the rectum and anus (plus or minus the sigmoid colon) and suturing over the anus. It leaves the patient with a permanent colostomy.

501
Q

What is Hartmann’s procedure?

A

Usually an emergency procedure that involves removal of the RECTOSIGMOID COLON and creating of a colosotmy.
The rectal stump is sutured closed
Colonostomy may be reversed later

502
Q

What is low anterior resection syndrome and what does it involve?

A

Low anterior resection syndrome may occur after resection of a portion of bowel from the rectum, with anastomosis between the colon and rectum. It can result in a number of symptoms, including:

Urgency and frequency of bowel movements
Faecal incontinence
Difficulty controlling flatulence

503
Q

Potential complications of surgery for bowel cancer?

A
Bleeding, infection and pain
Damage to nerves, bladder, ureter or bowel
Post-operative ileus
Anaesthetic risks
Laparoscopic surgery converted during the operation to open surgery (laparotomy)
Leakage or failure of the anastomosis
Requirement for a stoma
Failure to remove the tumour
Change in bowel habit
Venous thromboembolism (DVT and PE)
Incisional hernias
Intra-abdominal adhesions
504
Q

Follow up of bowel cancer post surgery?

A

Patients will be followed up for a period of time (e.g., 3 years) following curative surgery. This includes:

Serum carcinoembryonic antigen (CEA)
CT thorax, abdomen and pelvis

505
Q

What are the two main causes of acute cholangitis?

A

Obstruction in the bile ducts causing bile stasis (e.g. gallstones)
Infection introduced during an ERCP

506
Q

Most common caustive organisims of acute cholangitis?

A

Escherichia coli
Klebsiella species
Enterococcus species

507
Q

What is Charcot triad in acute cholangitis?

A

RUQ
Jaundice
Fever

508
Q

Management of acute cholangitis?

A
NBM
IV fluids
Blood culture
Antibiotics as per local guidelines
Involvement of seniors and potentially HDU or ICU
509
Q

Gold standard investigation for cholangitis?

A

ERCP (+interventional)

510
Q

How should a patient with acute cholangitis who has not responded to abx in the first 24hrs be managed?

A

Urgent billiary drainage

511
Q

Interventions that can be done during ERCP?

A

Cholangio-pancreatography: retrograde injection of contrast into the duct through the sphincter of Oddi and x-ray images to visualise biliary system
Sphincterotomy: making a cut in the sphincter to dilate it and allow stone removal
Stone removal: a basket can be inserted and pulled through the common bile duct to remove stones
Balloon dilatation: a balloon can be inserted and inflated to treat strictures
Biliary stenting: a stent can be inserted to maintain a patent bile duct (for strictures or tumours)
Biopsy: a small biopsy can be taken to diagnose obstructing lesions

512
Q

What is percutaneous transhepatic cholangiogram (PTC) used to manage?

A

Radiologically guided insertion of a drain through the skin and liver into the bile ducts, relieving immediate obstruction.
Stent can be used to give longer lasting relief
Used when ERCP has failed or for patients not suitable for ERCP

513
Q

How might acute cholecystitis present

A

RUQ pain, potentially radiating to right shoulder
Fever
Nausea
Vomiting
Tachycardia (fast heart rate) and tachypnoea (raised respiratory rate)
Right upper quadrant tenderness
Murphy’s sign
Raised inflammatory markers and white blood cells

514
Q

Signs of acute choleycystitis on USS

A

Thickened gallbladder wall
Stones or sludge in gallbladder
Fluid around the gallbladder

515
Q

What is Murphy’s sign and why and when does it occur?

A

Place a hand in RUQ and apply pressure
Ask the patient to take a deep breath in
The gallbladder will move downwards during inspiration and come in contact with your hand
Stimulation of the inflamed gallbladder results in acute pain and sudden stopping of inspiration

Acute cholecystitis

516
Q

If USS is not sufficient to visualised the billary tree what can be used?

A

Magnetic resonance cholangiopancreatography (MRCP)

517
Q

Management of gallbladder empyema?

A

Gallbladder empyema refers to infected tissue and pus collecting in the gallbladder. Management involves IV antibiotics and one of two main options:

Cholecystectomy (to remove the gallbladder)
Percutaneous cholecystostomy (inserting a drain into the gallbladder to allow the infected contents to drain)
518
Q

Complications of cholecysitis?

A

Sepsis
Gallbladder empyema
Gangrenous gallbladder
Perforation

519
Q

How is gallbladder empyema diagnosed?

A

USS

CT scan

520
Q

What does chronic cholecystitis increase the risk of?

A

Gallbladder carcinoma

Biliary enteric firstula

521
Q

How is chronic cholecystitis typically diagnosed?

A

CT imaging

522
Q

What is Bouveret’s Syndrome?

A

Inflammation of the gallbladder causes a fistula to form between the gallbladder wall and small bowel (cholecystoduodenal fistual)
A stone impacts in the proximal duodenum, causing a gastric outlet obstruction

523
Q

What is Gallstone Ileus?

A

Inflammation of the gallbladder causes a fistula to form between the gallbladder wall and small bowel (cholecystoduodenal fistual)
Stone impacts at the terminal illeum causing SBO?

524
Q

Cholangiocarcinoma is a type of cancer that originates in the bile duct, what is the most common?

A

Adenocarcinomas

525
Q

Where might cholangicarcinoma affect?

A

Intrahepatic bile ducts
Extrahepatic bile ducts
Perihiliar region most common (where right and left hepatic duct have joined to become the common hepatic duct)

526
Q

Key risk factor for cholangiocarcinoma?

A

Primary sclerosing cholangitis (risk factor for this is UC)

Liver flukes

527
Q

What is obstructive jaundice associated with?

A

Pale stools
Dark urine
Generalised itching

528
Q

What is the narrowest part of the small bowel?

A

Terminal ileum

529
Q

How might cholangiocarcinoma?

A
Jaundice (obstructive)
Unexplained weight loss
Right upper quadrant pain
Palpable gallbladder (swelling due to an obstruction in the duct distal to the gallbladder) - painless
Hepatomegaly
Pale stools
Dark urine
Generalised itching
530
Q

How is cholangiocarcinoma diagnosed?

A

Diagnosis is based on imaging (CT or MRI) plus histology from a biopsy.

531
Q

Why might MRCP and ERCP be used in cholangiocarcinoma?

A

Magnetic resonance cholangio-pancreatography (MRCP) may be used to assess the biliary system in detail to assess the obstruction.

Endoscopic retrograde cholangio-pancreatography (ERCP) can be used to put a stent in and relieve the obstruction, and also obtain a biopsy from the tumour.

532
Q

What tumour marker may be raised in cholangiocarcinoma?

A

CA 19-9

533
Q

If caught in the early stages, cholangiocarcinoma may be curatively treated - how?

A

Curative surgery +/- raidotherapy and chemotherapy

534
Q

Most cases of cholangiocarcinoma can not be cured, how is it managed palliatively?

A

Stents inserted to relieve the biliary obstruction
Surgery to improve symptoms (e.g., bypassing the biliary obstruction)
Palliative chemotherapy
Palliative radiotherapy
End of life care with symptom control

535
Q

Pancreatic cancer is often diagnosed late and has a very poor prognosis. The vast majority are what type of cancer?

A

Adenocarcinoma

536
Q

Pancreatic cancer is often diagnosed late and has a very poor prognosis. The vast majority are occur where?

A

Head of pancreas (as opposed to body and tail)

537
Q

The average survival of pancreatic cancer when diagnosed with advanced disease is only 6 months, why is prognosis so poor?

A

Pancreatic cancers spread and metastisise early

538
Q

Where do pancreatic cancers metastisise to?

A

Liver
Peritoneum
Lungs
Bones

539
Q

Why does pancreatic cancer cause obstructive jaundice?

A

Can compress the bile ducts when a tumour in head of pancreas grows large enough

540
Q

Presenting features of pancreatic cancer?

A
Yellow skin and sclera
Pale stools
Dark urine
Generalised itching
Non-specific upper abdominal or back pain
Unintentional weight loss
Palpable mass in the epigastric region
Change in bowel habit
Nausea or vomiting
New‑onset diabetes or worsening of type 2 diabetes
541
Q

Pancreatic cancer 2ww referal criteria?

A

Over 40 with jaundice – referred on a 2 week wait referral
Over 60 with weight loss plus an additional symptoms (Diarrhoea, back pain, abdo pain, nausea, vomiting, constipation – referred for a direct access CT abdomen)

542
Q

How is pancreatic cancer diagnosed?

A

Diagnosis is based on imaging (usually CT scan) plus histology from a biopsy.

543
Q

What investigations are used to stage pancreatic cancer?

A

Staging CT scan involves a full CT thorax, abdomen and pelvis (CT TAP). This is used to look for metastasis and other cancers.

544
Q

What tumour marker might be raised in pancreatic cancer?

A

CA 19-9 (carbohydrate antigen) is a tumour marker that may be raised in pancreatic cancer. It is also raised in cholangiocarcinoma and a number of other malignant and non-malignant conditions.

545
Q

What is the role of ERCP and MRCP in pancreatic cancer?

A

Magnetic resonance cholangio-pancreatography (MRCP) may be used to assess the biliary system in detail to assess the obstruction.

Endoscopic retrograde cholangio-pancreatography (ERCP) can be used to put a stent in and relieve the obstruction, and also obtain a biopsy from the tumour.

546
Q

How is biopsy taken in pancreatic cancer?

A

Percutaneous under ultrasound or CT guidance
During an endoscopy under ulrasound guidance
DUring ERCP

547
Q

Surgery may be used in early pancreatic cancer with small tumour size, what are the options?

A

Total pancreatectomy
Distal pancreatectomy
Pylorus-preserving pancreaticoduodenectomy (PPPD) (modified Whipple procedure)
Radical pancreaticoduodenectomy (Whipple procedure)

548
Q

Palliative treatment of pancreatic cancer?

A
Stents inserted to relieve the biliary obstruction
Surgery to improve symptoms (e.g., bypassing the biliary obstruction)
Palliative chemotherapy (to improve symptoms and extend life)
Palliative radiotherapy (to improve symptoms and extend life)
End of life care with symptom control
549
Q

What is Whipple Procedure?

A
Pancreaticoduodenectomy
Removal of:
Head of pancreas
Pylorus of stomach
Duodenum 
Gallbladder
Bile duct
Relevant lymph nodes
550
Q

What differs in a modified Whipple procedure?

A

A modified Whipple procedure involves leaving the pylorus in place. It is also known as a pylorus-preserving pancreaticoduodenectomy (PPPD).

551
Q

What does the gastrodudenal artery supply?

A

The gastroduodenal artery (GDA) is a terminal branch of the common hepatic artery which mainly supplies the pylorus of the stomach, proximal duodenum, and the head of the pancreas.

552
Q

Contraindications to liver transplant?

A

Significant co-morbidities (e.g., severe kidney, lung or heart disease)
Current illicit drug use
Continuing alcohol misuse (generally 6 months of abstinence is required)
Untreated HIV
Current or previous cancer (except certain liver cancers)

553
Q

What incision is used in liver transplant?

A

“rooftop” or “Mercedes Benz” incision along the lower costal margin for open surgery.

554
Q

What is an intra-abdominal abscess?

A

Intra-abdominal abscess is an intra-abdominal collection of pus or infected material, usually due to a localised infection inside the peritoneal cavity. It can involve any intra-abdominal organ or be located in between bowel loops, or be free within the peritoneal cavity itself.

555
Q

How do intra-abdominal abscess’ present?

A
Commonly presents with abdominal pain, fever, and leukocytosis
Also:
Fever or hypothermia
Abdominal pain
History of IBD
Tachycardia 
Change in bowel habits/abnormal bowel function
Prolonged ileus
Anorexia.lack of apetite
556
Q

What are intra-abdominal abscess’ usually secondary to?

A

Innoculation, commonly from complicated intra-abdominal infection (ie. bowel perforation, anastomtic leak, trauma)

557
Q

How is an intrabdominal abcess diagnosed?

A

USS, CTAP (usually more reliable and provided better delineation of anatomical location and abscess size)

558
Q

What are risk factors for an intraabdominal abscess?

A

diabetes
malignancy
recent surgery or trauma, appendicitis, diverticulitis, or perforated ulcer
male sex

559
Q

What investigations should be ordered first for intra abdominal abscess?

A

WBC count
drainage culture
abdominal CT scan

Also consider:
serum CRP
serum erythrocyte sedimentation rate (ESR)
Gram stain of abscess fluid
serum glucose
560
Q

How do anorectal abscess’ typically present?

A

Perianal pain and swelling

PR bleeding is uncommon - more suggestive of anal fissure

561
Q

What will an anorectal abscess appear like on examination?

A

Fluctuant tender peri-anal swelling

562
Q

If a anorectal abscess causes further infection what features might be present?

A

Pyrexia
Tachycardia
Sepsis - haemodynamic compromise

563
Q

Which patients typically present with a anorectal abscess?

A

Anorectal abscesses typically occur in men age 20-40 years old.

564
Q

What are the risk factors for anorectal abscess?

A

Anal fistulae
Crohn’s disease
Male sex

565
Q

How are anorectal abscesses managed?

A

Drainage, to prevent spread of infection and sepsis
Either in A&E under local anaesthetic
Or in theatre if deep with sphincter extension

566
Q

What causes a pilonidal abscess?

A

Pilonidal disease is caused by insertion of hairs into the skin of the natal cleft, at the sacrococcygeal region. This causes a chronic inflammatory response, with formation of a discharging sinus. Infection of the region may precipitate abscess formation.

567
Q

How does pilonidal abscess usually present?

A

Pilonidal disease typically occurs in male patients age 15-40 and is more common in the presence of thick stiff body hair (especially patients who sit down a lot e.g. lorry drivers)

Patients typically present with offensive discharge from the natal cleft and discomfort, especially when seated.

On physical examination sinus tracts may be visible around the natal cleft.

If superinfection occurs, there may be abscess formation which results in a tender fluctuant swelling and low-grade fever.

568
Q

What is a subcutaneous abscess?

A

A subcutaneous abscess is a kind of soft tissue abscess and a manifestation of a spectrum of skin and soft tissue infections which also includes cellulitis and necrotizing fasciitis. It is a form of abscess which lies within the dermis and subdermal cutaneous layers. Along with dental abscesses, the subcutaneous layer is the most common site for abscess formation.

569
Q

How does a subcutaneous abscess typically present?

A

Patients typically present with an acute or subacute history of a focal swelling or lump in the affected skin with accompanying signs of cellulitis.

If there is bacteremia, the patient may present with systemic signs of sepsis such as fever, rigours, and raised inflammatory markers.

570
Q

What is the most common caustive pathogen of a subcutaneous abscess?

A

Steptococcus species

571
Q

Pathology of subcutaneous abscess formation?

A

Skin abscesses are overwhelmingly caused by bacteria that spread into the subcutaneous tissues through breaches in the epidermis.

In some cases sterile abscess formation has been described where an irritant drug or substance is injected into the skin, resulting in aseptic inflammation and abscess formation.

572
Q

Subcutaneous abscess is usually diagnosed clinically, why might imaging be used and what imaging is the prefered modaility for the evaluation of more deep soft tissue abscess?

A

If radical surgical treatment is being considered imaging may be undertaken to determine the extent of soft tissue involvement.

MRI

USS can also be useful for differntiating cellulitis with gross cutaneous swelling from a true abscess

573
Q

Differential diagnosis for subcutaneous abscess?

A
lymph node enlargement
sebaceous cyst
seroma
lymphocele
hematoma
herniated bowel
blood vessel
574
Q

Risk factors for subcutaneous abscess?

A
Advanced age
Trauma
DM
Mallignancy
Immunocompromised state
Obesity
575
Q

How do you manage subcutaneous abscess?

A

Incision and drainage is the definitive treatment of a soft tissue abscess.

However, premature incision before localization of pus will not be curative and may be deleterious.

In cases of immature abscesses or cellulitis, oral antibiotics and warm compresses may be of value in helping the infection to coalesce.

576
Q

How is Meckel’s diverticulum most accurately diagnosed?

A

99 Technetium scan

577
Q

What incision is used in an emergency c section?

A

Pfannenstiel’s

578
Q

What incision is used in bile duct exploration?

A

Kocher’s

579
Q

What incision is used in Whipple procedure

A

: Rooftop or Midline

580
Q

What is Rigler’s sign?

A

Rigler’s sign: 2 lines of the intestinal surface is seen on abdominal x ray

581
Q

How might a minor internal haemorrhoid be managed?

A

The correct answer is: Topical dilti

582
Q

Initial management of an anal fissure?

A

Initial therapy should be with pharmacological agents to relax the sphincter and facilitate healing. This is particularly true in females presenting for the first time.

583
Q

How should recurrent episodes of natal cleft pain with discharge be managed?

A

Pilonidal cystectomy

584
Q

How does a strangulated femoral hernia present?

A

colicky abdominal pain and a tender mass in the groin.

585
Q

How should a thrombosed haemorrhoid be managed if it presents after 72 hours?

A

Following the first 72 hours of acute thrombosis, the thrombus is likely to organise and contract- lessening symptoms and typically self-resolving within a few weeks. In such scenario, it is more appropriate to offer conservative management options including analgesia, stool softeners and using ice-packs to reduce pain.

586
Q

How should a thrombosed haemorrhoid be managed in the first 72 hrs?

A

If a patient with thrombosed haemorrhoids presents within 72 hours of onset of the pain, NICE recommends offering admission for surgical management of the piles. This provides immediate pain relief.

587
Q

How do thrombosed haemorrhoids present?

A

Thrombosed haemorrhoids are characterised by anorectal pain and a tender lump on the anal margin

588
Q

What can a gastrectomy lead to subacute combined degeneration of the spinal cord (loss of vibration sense, hyperreflexia, and absent reflexes)

A

Gastrectomy may result in vitamin B12 deficiency

589
Q

Why do post-gastrectomy patients not immediatley suffer vitamin deficiency?

A

B12 stores can last a couple years.

Folate lasts couple months

590
Q

What imbalances might a high output stoma cause?

A

These patients may develop significant volume depletion, electrolyte and acid-base disturbances (metabolic acidosis) if the ileostomy output increases or if dietary intake is disrupted or altered. Hence, it is important to monitor fluid balance including stoma output in these patients.

591
Q

Inestigatio of choice for Boerhaaves syndrome?

A

CT contrast swallow is the investigation of choice for suspected Boerhaave’s syndrome

592
Q

How is a pancreatic pseudocyst usually managed?

A

Conservatively

593
Q

Causes of pancreatitits?

A

Gallstones
Ethanol
Trauma
Steroids
Mumps (other viruses include Coxsackie B)
Autoimmune (e.g. polyarteritis nodosa), Ascaris infection
Scorpion venom
Hypertriglyceridaemia, Hyperchylomicronaemia, Hypercalcaemia, Hypothermia
ERCP
Drugs (azathioprine, mesalazine*, didanosine, bendroflumethiazide, furosemide, pentamidine, steroids, sodium valproate)

594
Q

Most commonly performed operation for rectal tumour?

A

Anterior resection is the most commonly performed operation for rectal tumours, except in lower rectal (tumours abdominoperineal excision of rectum is for low rectal or anal tumours)

595
Q

Diverticulitis symptoms + vaginal passage of faeces or flatus suggest what?

A

Diverticulitis symptoms + vaginal passage of faeces or flatus → ?colovaginal fistula

596
Q

What type of cannula does a haemodynamically stable pt require?

A

only require intravenous access temporarily a 20 G (pink) peripheral cannula will suffice.

597
Q

Pigmented gallstones are associated with which conditon?

A

Pigmented gallstones are associated with sickle cell

598
Q

How does gastric volvulus present?

A

Gastric volvulus- triad of vomiting, pain and failed attempts to pass an NG tube

599
Q

What is the first-line medication for primary biliary cholangitis?

A

Ursodeoxycholic acid

600
Q

Surgical management of splenic flexure tumour?

A

Left hemicolectomy

601
Q

Surgical management of UPPER RECTAL TUMOURS?

A

Anterior resection and colo-rectal anastomosis

602
Q

Surgical management of lower rectal tumour?

A

Abdomino-perineal excision of rectum

603
Q

Organisms causing post splenectomy sepsis?

A

Streptococcus pneumoniae
Haemophilus influenzae
Meningococci

604
Q

If a patient with ulcerative colitis has had a severe relapse or >=2 exacerbations in the past year they should be given what to maintain remission?

A

either oral azathioprine or oral mercaptopurine