GI Flashcards

(343 cards)

1
Q

How do you take an abdominal pain history?

A

https://geekymedics.com/gi-history/

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2
Q

Site abdo pain examples

A

Epigastric pain/acute abdo - pancreatitis, gastro duodenal ulcers, perforation
Groin lump - hernias
RIF - appendicitis
LIF - IBD, diverticular disease
RUQ - gallstones
From epigastric to whole of abdomen- peritonitis (if spread to chest then cardiac)
Other - intestinal obstruction, stoma’s

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3
Q

Onset epigastric pain examples

A

Sudden - perforation of viscus (like ulcer)
Maximal intensity at 10-20 mins - acute pancreatitis or billary colic
Maximal intensity at Hours - cholecystitis, hepatitis, pneumonia

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4
Q

Epigastric pain character examples

A

Crushing or tight - cardiac (spread ro jaw neck and arm)
Sharp/burning - peptic Ucler, gastritis, duodenitis
Deep ‘boring’ - pancreatitis (with spread to back)
Retrosternal - oesophagitis

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5
Q

Relieving and aggravating factors epigastric pain examples

A

Sitting forward - acute pancreatitis better
Eating - duodenal better and gastric worse
Movements - peritonitis worse
Deep breathing - pleural inflammation worse
Fatty meals - billary colic worse

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6
Q

Which epigastric pain conditions are likely to present to hospital?

A

Pancreatitis, perforated peptic ulcer and MI

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7
Q

What other symptoms are common with epigastric pain?

A

Nausea/vomit - acute pancreatitis amd inferior MI(irritation of diaphragm)
After vomit - pain - boerhaave’s syndrome - perforation of oesophagus
Fever - infection - hepatitis or peritonitis
Dyspepsia- heartburn, bitter taste - GORD
Change in stool - pale - bile blocked or if stetorrhea so float, pale and foul smell - pancreatic exocrine insuffiency or billary disease
Cough - basal pneumonia

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8
Q

How do you perform an abdo exam?

A

https://learn-eu-central-1-prod-fleet01-xythos.content.blackboardcdn.com/5bfe8efc36910/2138481?X-Blackboard-Expiration=1661709600000&X-Blackboard-Signature=KltoaT1A5woXZmZBxdU8wbjCWuyWLnQAwInxlDTlLI4%3D&X-Blackboard-Client-Id=160309&response-cache-control=private%2C%20max-age%3D21600&response-content-disposition=inline%3B%20filename%2A%3DUTF-8%27%27Examination%2520Checklists%2520-%2520Cardiovascular%252C%2520Respiratory%252C%2520GI%252C%2520CNS%2520%2528Cranial%2520and%2520Peripheral%2529%2520%25282%2529.pdf&response-content-type=application%2Fpdf&X-Amz-Security-Token=IQoJb3JpZ2luX2VjEI3%2F%2F%2F%2F%2F%2F%2F%2F%2F%2FwEaDGV1LWNlbnRyYWwtMSJGMEQCIDSmSZ8oiE52YgmYZLM%2FDu6URxmEi%2Fo%2BZ3RmeH6mp%2BXqAiANbVsFDKZMpZgfMpO3Xh2n5edXNmTty4m8KDrq%2B7tncSrcBAgWEAIaDDYzNTU2NzkyNDE4MyIMvkVPrVPr%2FqjIgu2gKrkEKlGdVedOq%2Bh1nhykOXA6EPzl3%2F%2FU5ZCMweyMcfOE2phDzJtQoCGf2CpsIOHKoCrwEq7ON7e%2F%2ButXjYeD61oxEheoXPTe4Jq5glJz3gH177qwiInl6%2B%2Fg9Ys1AMoguPJX%2FoH4UjuhzUQ%2F77p%2Fmn6NbYYjQSSZyCEAEC5ADdd5SFIzc%2FCF58Rfn9kcHQ7JQB66g3K4C%2BfDPJX5MU8ZkYMiueFGsjBmES%2FcAKNjpM5rg3PskqQJtYDWKBMz20C9LE4XK17JWBt3L9qhHs%2FPbFmZpFJ9L2UxC5%2BzbNDh7HybcDJ71VG30e8aaDD7H%2BWiEPjaPYO6M5xKJDJNJyB1hE0WPdDspj4%2FuxCDEbBlfLVHqkE%2FH477ynrVwY37wQjsBWsvKq4bbcpOV1QmChCtYLl%2BbSeBJPaGjnd6d%2FNuLOomTZkjJj5aomMccWP0U45Q7qZDKCwDiXcXFODdiCPBIU5BxgHIwy6rkE0fU2KE%2Bwyu5HS3VEpeEmRxlFmqKdPqOI%2BLctgrh1%2BtWfaRam5r1Di2YhClSaw5Oe%2Bp7aXAvB0rQLv04VETbGXnIBzag7RklokN2whTCc7hWR8l9JSYC3bmvj3Fc0XnBHQPjHUrdOuXB%2B7DlHN3ykRb5G7tNC0CIrPCZphhxJA2FeJ%2FgnujP6ZIM6il05uftcJybUUlE0erFucXcciwxjU6MlNXVt5U7PMcliUL5421%2B2DEqQ9kdleZidkfvmGFhyO%2BgxGxc2OFmU4gdfjRrOPcXzEwxNStmAY6qgFJqtFnWKU3L282Tsyx5A4HOWD9U2MmepYAKxDQ5jGlEPg7lzsiGuNVlYKeoEVVEcdX0s%2BMQVcMEgsxbbK4JRvh5UIwHQcV7haHVxX0yPa7dJkcYG59Qhnov%2BpNklLn4HzSGxhyGNue1VVnxzx5CNBP1osGH8gGE1CF%2F4Jk20r828SPkYMJEMAdreRBk9GkZdVdLAx5%2BWgBBKzWtX8%2FL1BDROLOI0l9e1mpQQ%3D%3D&X-Amz-Algorithm=AWS4-HMAC-SHA256&X-Amz-Date=20220828T120000Z&X-Amz-SignedHeaders=host&X-Amz-Expires=21600&X-Amz-Credential=ASIAZH6WM4PL7LRB5MCL%2F20220828%2Feu-central-1%2Fs3%2Faws4_request&X-Amz-Signature=7b6ab6eb065679004e4923c58c76396ede6f9f1407044089ee918300dfeca4f8

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9
Q

What are common acute surgical conditions?

A

Intestinal obstruction
Rupture AAA
Ruptured ectopic pregnancy
Bleeding gastric ulcer
Peritonitis
Ischaemic bowel

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10
Q

What is the common presentation for intestinal obstruction?

A

Small bowel - peri umbilical pain suddenly, (early) nausea and vomit, abdo tender and distended, more younger
High pitched bowel sounds, absolute constipation
Large bowel - periumbilical pain, abdo tender and distended, N+V, constipation then diarrhoea, older

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11
Q

How do you manage an intestinal obstruction?

A

Diagnosed - x ray - distended loops peripherally or centrally
Air enema or surgery

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12
Q

What are the causes of an intestinal obstruction?

A

Small bowel - intra abdominal adhesions (fibrous bands between organs or tissues or both), prior surgery, incarcerated hernias, meckels diverticulum, strictures from crohns, tumours, foreign body
Large - colorectal cancer, caecal or sigmoid Volvulus, strictures from diverticulitis

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13
Q

What are the common presentations of an upper GI haemorrhage?

A

Haematemesis - coffee ground like as partially digested blood
Altered bowel habits - dark tarry stools (malaena) or haematochezia - fresh blood
Epigastric abdo pain
Syncope due ro hypovolaemia or cerebral hypoperfusion
Tachycardia
Hypotension

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14
Q

How do you manage an upper GI haemorrhage?

A

FBC UE
Endosocpy
Prophylactic antibiotics
Medication

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15
Q

What are the common causes of an upper GI haemorrhage?

A

Peptic ulcer
Mallory-Weiss tears
Varices
Oesophagitis

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16
Q

What are the common presentations of stomach cancer?

A

Similar pain to peptic ulcer

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17
Q

How do you manage a patient with stomach cancer?

A

FBC, tumour markers,X ray, CT/MRI, endoscopy/colonscopy, TNM, Duke’s
Surgical resection, chemo, radio, palliative

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18
Q

What are the causes of stomach cancer?

A

Smoker, high diet, h.pylori, men, FHx

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19
Q

How does oesophageal cancer present?

A

Dysphagia
Epigastric pain
Malaena
Haematemesis

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20
Q

How do you manage oesophageal cancer?

A

FBC, tumour markers,X ray, CT/MRI, endoscopy/colonscopy, TNM, Duke’s
Surgical resection, chemo, radio, palliative

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21
Q

What are the common presentations of HPB?

A

Hepato - hepatomegaly, jaundice, unintentional weight loss, painless, ascites
Pancreatic - jaundice, vague symptoms

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22
Q

What is the management of HPB cancer?

A

FBC, tumour marker (CA19-9 - pancreatic)X ray, CT/MRI, endoscopy/colonscopy, TNM, Duke’s
Surgical resection, chemo, radio, palliative

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23
Q

What are the causes of HPB cancer?

A

men, fh, smoker! chronic pancreatitis

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24
Q

What are the presentations of colorectal cancer?

A

Unintentional weight loss, unexplained abdo pain, PR bleeding,, change in bowel habitn(ride sided - late change, left -early), anaemia, tenesmus

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25
What is the management of colorectal cancer?
FBC, tumour marker (CEA), X ray, CT/MRI, endoscopy/colonscopy, TNM, Duke’s Surgical resection, chemo, radio, palliative
26
What are the causes of colorectal cancer?
FHx, IBD, polypodies syndrome, diet snd lifestyle (low fibre), coeliac (small)
27
What is the common presentation of different hernias?
Not incarcerated - fullness/swelling, gets larger when intra abdo pain increases, aches Incarcerated - pain, nor moveable, N+V, symptomatic sx if ischaemic
28
What is the management of hernias?
Reduce it and cut out any ischaemia bowel
29
What are the causes of hernias?
Weakness in cavity - congenital (if processes vaginalis doesn’t close - connection from peritoneal cavity to scotum), post surgery, Increases in abdo pressure - obesity, weightlifting, constipation/cough, pregnancy
30
What is the presentation of gallstones?
RUQ - shoulder tip Complication - billary colic - RUQ pain after eating fatty pain, acute cholecystitis - murphy’s sign, acute ascending cup,angitis - pain, inflammation and jaundice (Charcot)
31
What is the management of gallstones?
USS (radio lucent), analgesia, biliary colic and acute cholecystitis- elective cholecystectomy, ascending cholangitis - Iv antibiotics, fluid amd relieve obstruction
32
What are the causes of gallstones?
High cholesterol, overweight, 40\5., woman, pregnancy,
33
What are the common presentations of acute pancreatitis?
Epigastric pain radiating to back, vomit, Cullen and Grey turners
34
What is the management of acute pancreatitis?
CR/MRI to detect necrosis, raised lipases Fluids and organ support
35
What are the causes of acute pancreatitis?
Gallstones, alcohol, trauma, steroids, mumps, autoimmune, hyperlipidaemia, drugs
36
What are the presentation f intrahafominap/subcutaneous and peri anal abscess or sepsis?
37
What is the management of a patient with an abscess/sepsis?
38
What are the causes of abscess/sepsis?
39
What are the common presentations requiring a stoma?
40
What is the initial management with a stoma?
41
How are wounds managed?
42
Why might someone require a stoma?
43
What are the causes of oesophageal cancer?
Smoker, Barrett’s
44
what is the pathophysiology of a bowel obstruction?
mechanical blockage of bowel..gross dilation of proximal limb of bowel...increased peristalysis, secretion of electrolyte rich fluid into bowel
45
what is the most common cause of bowel obstruction - small bowel - large bowel?
small - adhesions and hernia large - malignancy, diverticular disease and volvulus
46
what are the causes of bowel obstruction -intraluminal -mural -extramural?
intraluminal - gallstone ileus, foreign body, faecal impaction mural - cancer, strictures, intessusception, meckel's diverticulum,lymphoma extramural - hernia, adhesion, volvulus
47
what are the cardinal features of bowel obstruction?
abdo pain -colicky or cramp vomit - early if proximal and late if distal constipation - vice versa distension
48
what may be found on examination of someone with bowel obstruction?
distension cachexia - malignancy previous surgical scars hernia tympanic sound on percussion tinkling bowel signs
49
differentials for bowel obstruction
paralytic ileus toxic megacolon constipation
50
which investigations are required for suspected bowel obstruction?
urgent bloods - fbc, ue (lots of third space losses), crp, lfts and group and save venous blood gas - lactate shows signs of ischaemia imaging - CT with contrast of abdo and pelvis, may use abdo x ray (>3cm in small, >6cm in large, >9cm in caecum)
51
how do small and large bowel look different on x ray?
small - central, valvulae conniventes (completely cross bowel ) large - peripheral, haustra (halfway)
52
what is the initial management of a patient with bowel obstruction?
IV fluid rescusitation (to drip) urinary catheter NBM NG tube (and suck - to decompress bowel) analgesia and anti emetics
53
what are some red flag sx of bowel obstruction indicative of ischaemia?
focal tenderness, pyrexia and pain worse on movement #
54
how is the management of bowel obstruction decided?
if previous surgery resulting in adhesion - treated conservatively unless evidence of ischaemia if not resolves within 24 hrs with conservative management...water soluble contrast...not reach colon by 6 hours..surgery if not had surgery and has obstruction - usually requires surgery if needs surgical correction, ie strangular hernia - surgery fails to improve within 48 hours -surgery
55
what are the 3 most common complications of bowel obstruction?
bowel ischaemia bowel perforation dehydration
56
define melena
black tarry stools with offensive smell - upper gi bleed..alteration and degradation of blood by digestive ienzymes
57
define melena
black tarry stools with offensive smell - upper gi bleed..alteration and degradation of blood by digestive ienzymes - PID, liver disease and gastric cancer...confirmed by DRE
58
how can liver cirrhosis result in melena?
varices- dilation of the porto-systemic anastomses in oesophagus...due to portal hypertension secondary to liver cirrhosis which can rupture
59
what features are important to ellicit in a patient with melena?
colour and tecture abdo pain, dyspepsia, dysphagia smoking/alcohol steroids, nsaids, anticoag
60
which investigations are required for melena?
FBC, UE, LFT, clotting - drop in Hb, Liver damage, rise in urea:creatinine ratio group and save and 4 units cross matched ABG OGD or CT abdo with contrast
61
how is melena managed?
A to E approach if PID = injections of adrenaline and cauterisation, high dose PPI IV if varices - endoscopic banding, prophylactic abx, somatostain analogue (reduce splanchnic blood flow), tube inserted to compress bleeding if GI malignancy - biopsies, surgical/oncological management - may require blood transfusion and correction of coagualtion
62
what are the causes of Gi perforation?
diverticulitis PUD Gi malignancy iatrogenic - endoscopy trauma foreign body appendicits or meckel's diverticulum mesenteric ischaemia toxic mgacolon excess vomiting
63
what are the clinical features of GI perforation?
pain is rapid and sharp systemically unwell malaise vomit lethargy features of peritonism - localised, generalised rigid abdomen
64
which investigations are required for perforation?
FBC, UE, LFT, clotting, G and S usually raised WCC + CRP CT scan - free air
64
which investigations are required for perforation?
FBC, UE, LFT, clotting, G and S usually raised WCC + CRP CT scan - free air
64
which investigations are required for perforation?
FBC, UE, LFT, clotting, G and S usually raised WCC + CRP CT scan - free air
64
which investigations are required for perforation?
FBC, UE, LFT, clotting, G and S usually raised WCC + CRP CT scan - free air
64
which investigations are required for perforation?
FBC, UE, LFT, clotting, G and S usually raised WCC + CRP CT scan - free air
64
which investigations are required for perforation?
FBC, UE, LFT, clotting, G and S usually raised WCC + CRP CT scan - free air
65
how is gi perforation managed?
broad spectum abx NBM NG tube IV fluid resuscitation analgesia repair of perforated viscus and washout localised diverticular perforation and sealed upper gi perforation and elderly patients - conservative
66
what presentations require urgent intervention?
bleeding so in hypovolaemic shock- ruptured AAA- refer to vascular team and immediate surgery - ruptured ectopic pregnancy - bleeding gastric ulcer - trauma perforated viscus = peritonitis - peptic ulceration - obstruction - diverticular disease - IBD lay still, tachy and hypo, rigid abdomen, involuntary guarding, reduced bowelsounds ischaemic bowel - severe out of proportion, raised lactate, diffuse pain,CT with contrast others which are less acute - colic - can not get comfortable - peritonism (not peritonitis)
67
which investigations are required for acute abdo pain?
urine dipstick - infection, haematuria, preg ABG - septic or bledding routine blood - fbc, ue,lft, crp, amylase,group and save blood cultures - infection imaging - erect chest x ray for free air - USS for KUB - hydronephrosis, nilliary tree and liver for gallstones, transvaginal for tubo-ovarian pathology - possible CT
68
what is the general management of acute abdo pain?
IV access - large bore cannulas NBM analgesia anti emetics imaging VTE prophylaxis urine dip bloods catheter NG tube Iv fluids
69
what are the emergency causes of haematemesis?
oesophageal varices gastric ulceration
70
what are the non emergency causes of haematemesis?
mallory-weiss tear oesophagitis gastritis gastric malignancy meckel's diverticulum
71
define oesophageal varices
porto systemic venous anastomoses in oesophagus dilated veins prone to rupture common underlying cause - alcoholic liver disease
72
what is the first line investigation of a patient with haematemesis and history of alcohol abuse?
URGENT OGD
73
where can gastric ulceration most commonly occur?
blood vessels supplying: lesser curve of stomach posterior duodenum
74
define mallory weiss tear
forceful vomiting causes a tear in epithelial lining of the oesophagus most cases benign but if prolonged - OGD
75
what are the causes of oesophagitis?
GORD infections such as candida albicans medications - bisphosphonates radiotherapy ingestion of toxic substances crohns disease
76
what features are important in a history with haematemesis?
timing, frequency, volume history of dyspepsia, dysphagia past medical hx and smoking and alcohol use of steroids, nsaids, anticoagulations, bisphosphonates
77
which investigations are required for haematemesis?
fbc may not show anaemia LFT - liver damage group and save and 4 units cross matched OGD chest x ray - pneumoperitoneum
78
what system is used to risk stratify patients admitted with upper GI bleed?
glasgow-blatchford bleeding score
79
how are patients with haematemesis managed?
rapid A->E -2 large bore Iv cannulas - fluid resuscitation - crossmatch blood - OGD
80
how is peptic ulcer managed?
injections of adrenaline, cauterisation of bleeding high dose PPI H.pylori eradication
81
how is oesophageal varices managed?
blood products prophylactic abx endoscopic banding somatostatin analogues or vapressors
82
how is an active bleed managed?
angio-embolisation
83
what are the causes of dysphagia?
oesophageal malignancy benign strictures extrinsic compression - thyroid pharngeal pouch foreign body post stroke achalasia myasthenia gravis MS
84
what is the medical term for pain when swallowing?
odynophagia
85
what sx do you need to ask about with a patient who has dysphagia?
regurgiation sensation of food getting stuck hoarse voice weight loss referred ear or neck pain
86
which investigations are required for dysphagia?
endoscopy +- biopsy FBC, LFT barium swallow
87
define gastric outlet obstruction
mechanical obstruction between gastric pyloris and proximal duodeum so stomach can not empty
88
what are some causes of gastric outlet obstruction?
peptic ulcer, gastric cancer/small bowel cancer, iatrogenic
89
what are the clinical features of a patient presenting with gastric outlet obstruction?
epigastric pain postprandial vomiting early satiety dehydrated hypovolaemic tachycardic tender upper abdomen
90
medical term for delayed gastric empyting
gastroparesis
91
which investigations are required for gastric outlet obstruction?
fbc, crp, ue, clotting, group and save abdo x ray or CT with contrast endoscopy
92
how is gastric outlet obstruction managed?
resuscitation fluids catheter NG tube to decompress stomach IV PPI endocopy can dilate surgery if all else fails
93
what are some lower GI causes of rectal bleeding?
diverticular disease, ischaemic or infective colitis, haemorrhoids, malignancy, crohn's or UC
94
define haemorroids
engorged vascular cushions in the anal canal
95
what are important to ask in a hx with per rectal bleeding?
duration,frequency, colour, relation to stool and defecation associated sx family hx of bowel cancer or IBD
96
which investigations are required for per rectal bleeding?
bloods - fbc, ue, lft, clotting, group and save stool culture - rule out infective cause urgent CT angiography if haemodynamically unstable flexible sigmoidoscopy - left colon malignancy OGD
97
how is per rectal bleeding managed?
unstable rectal bleeding (less common) - A->E, IV fluids, blood products any Hb<70 - red cell transfusion endoscopic haemostasis - injected diluted adrenaline arterial embolisation possible surgical tx
98
what are the risk fx for GORD
age, obesity, male, alcohol, smoking, caffeine/spicy
99
what are the risk fx for GORD
age, obesity, male, alcohol, smoking, caffeine/spicy
99
what are the risk fx for GORD
age, obesity, male, alcohol, smoking, caffeine/spicy
100
what are the clinical features of GORD
chest pain burning retrosternal sensation worse after meals, lying or bending over relieved by antacids possible - belching, odynophagia, chronic cough
101
what are the red flag symptoms for GORD?
dysphagia weight loss early satiety malaise loss of appetite
102
what is GORD a risk fx for?
barretts oesophagus
103
what red flag sx required urgent endoscopy?
dysphagia >55 with upper abdo pain, weight loss, dyspepsia,reflux
104
what investigations are required for GORD and when would you consider investigating?
endoscopy - worsen depsite PPI, new onset and in older pts 24 hr pH monitor is gold standard for GORD + manometry to exclude dysmotility
105
how do you manage GORD?
conservative - less caffeine, weight loss, smoking cessation, PPI
106
what are the indications for surgery in GORD?
failure to response, patient preference, with complications - recurrent pneumonia
107
how is GORD handled surgically?
fundoplication - fundus wrapped around GOJ
108
what are the main complications of GORD?
aspirational pneumonia, barrets, strictures, cancer
109
what are the risk factors for squamous cell carcinoma?
middle and upper thirds - smoking and alcohol achalasia
110
what are the risk factors for adenocarcinoma?
lower third (usally barretts) LONG STANDING gord OBESITY HIGH FAT INTAKE
111
what are the clinical features of oesophageal cancer?
dysphagia weight loss odynophagia hoarseness supraclavicular lymphadenipathy
112
which investigations are required for oesophagus cancer?
OGD within 2 week, biopsy staging - CT CAP, endoscopic USS, staging laproscopy
113
how is squamous cell v adenocarcinoma treated?
scc - chemo - radiation adeno -neoadjuvant chemo or chemo radiotherapu following resection
114
what is the main surgical management for oesophageal cancer?
oesophagectomy - removes tumour, top of stomach, surrounding lymph nodes ivor lewis or mckeon procedure
115
whaat is post op function post oesophagectomy?
lose the reservoir function of the stomach. Many centres will routinely insert a feeding tube into the small bowel (a “feeding jejunostomy”) to aid nutrition. However, most patients will need to eat 5-6 small meals per day to meet their nutritional requirements.
116
whaat is post op function post oesophagectomy?
lose the reservoir function of the stomach. Many centres will routinely insert a feeding tube into the small bowel (a “feeding jejunostomy”) to aid nutrition. However, most patients will need to eat 5-6 small meals per day to meet their nutritional requirements.
117
prognosis of oesophageal cancer
poor - 5-10% as late presentation
118
define oesophageal perforation
full thickness rupture if spontaenous - boerhaave's syndrome
119
define oesophageal perforation
full thickness rupture if spontaenous - boerhaave's syndrome Perforation will result in leakage of stomach contents into the mediastinum and pleural cavity, which triggers a severe inflammatory response which will rapidly become overwhelming, resulting in a physiological collapse, multi-organ failure, and death.
120
what are the clinical features of oesophageal perforation?
retrosternal chest pain, resp distess, subcutaneous emphysema
121
which investigations are required for oesophgeal perforation?
routine bloods chest x ray - pneumoperitoneum CT chest abdo pelvis with contrast
122
what is involved in the initial management of oesophageal perforation?
septic and require urgent fluid resus
123
what are the indications for surgical management of oesophageal perforation and what surgery?
spontaneous perforation thoractomy to control leak and wash out chest
124
how is oesophageal perforation managed non surgically and the inidcations?
iatrogenic tend to be more stable or if too frail/co morbidities to undergo surgery Initial suitable resuscitation and transfer to Intensive Care / High Dependency Unit Appropriate antibiotic and anti-fungal cover Nil by mouth for 1-2 weeks, with endoscopic insertion of an NG tube on drainage Large-bore chest drain insertion Total Parenteral Nutrition (TPN) or feeding jejunostomy insertion
125
what is the prognosis of oesophageal perforation?
mortality and morbidity high
126
define mallory weiss tear
lacerations in mucosa usually at GOJ after profuse vomiting short period of haemaetemsis managed conservatively
127
the anatomy of the oesophagus
The upper oesophageal sphincter is comprised of skeletal muscle, and prevents air from entering the GI tract. The lower oesophageal sphincter (LOS) is composed of smooth muscle, and prevents reflux from the stomach. Peristaltic waves, controlled by the oesophageal myenteric neurones, propel ingested food down the oesophagus. The primary wave is under control of the swallowing centre and the secondary wave is activated in response to distention.
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define achalasia
failure of relaxation of LOS and absence of peristalysis along oesophagus increased risk of cancer
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what are the clinical features of achalasia?
progressive dysphagia for solids and liquids regurgitation resp complications, chest pain, dyspepsia,weight loss
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which investigations are required for suspected achlasia?
OGD - cancer oesophageal menometry - Absence of oesophageal peristalsis Failure of relaxation of the lower oesophageal sphincter High resting lower oesophageal sphincter tone
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conservatyive management of achalasia
sleep with pillows, eating slowly, chewing, fluids
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medical management of achalasia
calcium channel blockers - inhibit LOS contraction botox due to LOS via endoscopy
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surgical management of achalasia
Laparoscopic Heller Myotomy* – the division of the specific fibres of the lower oesophageal sphincter which fail to relax (Fig. 4), often seen as the A long-term improvement in swallowing is seen in ~85% of patients, with lower side-effect profile compared to endoscopic treatment Per Oral Endoscopic Myotomy (POEM) – a cardiomyotomy at the LOS is performed from the inside of the oesophageal lumen, through a submucosal tunnel Endoscopic Balloon Dilatation – insertion of a balloon into the lower oesophageal sphincter, which is dilated to stretch the muscle fibres or well patients with type II pattern by HRM Those with end-stage refractory achalasia may eventually require an oesophagectomy.
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define diffuse oesophageal spasm
dysfunction of oesophageal inhibitory nerves
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what are the clinical features of diffuse oesophageal spasm?
severe dysphagia to solids and liquids central chest pain will respond to nitrates unlike angina pectoris
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which investigations are required for diffuse oesophageal spasm?
manometry - repetitive, simulatenous and ineffective contractions endoscopy
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how is DOS managed?
relax oesophageal smooth muscle via CCB pneumatic dilation and heller myotomy - surgery
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what are some other causes of oesophageal dysmotility?
autoimmune CT disorders
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how is a hiatus hernia classified?
sliding (80%) - GOJ, abdo part of oesophagus and cardia of stomach move upwards through diaphragmatic hiatus into thorax rolling or para-oesophageal (20%) - upward movement of gastric fundus occurs to lie alongside a normally positioned GOJ..bubble
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what are the risk fx for developing a hiatus hernia
age related loss of diaphragmatic tone, increased abdo pressure, increased size of diaphragmatic hiatus, pregnnacy, obesity, hiatus
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what are the clinical features of a hiatus hernia?
vast are asx GORD sx, vomit, weight loss, bleeding/anaemia, hiccups, palpitations, swallowing difficulties bowel sounds may be auscultated within chest
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which investigations are required for hiatus hernia?
OGD or incidentally on CT/MRI
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conservative management of hiatus hernia
PPI with food weight loss alteration of diet smoking cessation reduce alcohol
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how is a hiatus hernia managed surgically>
Cruroplasty – The hernia is reduced from the thorax into the abdomen and the hiatus reapproximated to the appropriate size. Any large defects usually require mesh to strengthen the repair. Fundoplication – The gastric fundus is wrapped around the lower oesophagus and stitched in plac
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what are the indications for surgery of a ahiatus hernia?
Remaining symptomatic, despite maximal medical therapy Increased risk of strangulation/volvulus* (rolling type or mixed type hernia, or containing other abdominal viscera) Nutritional failure (due to gastric outlet obstruction)
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what are some specific complications of a hiatus hernia surgery?
recurrence of hernia bloating dysphagia if fundoplication too tight fundal necrosis - blood supply via left gastric artery and short gastric vessels have been disrupted
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define gastric volvulus and the triad involved
stomach twists on itself by 180 degrees, leading to obstruction of gastric passage and tissue necrosis bouchardt's triad - severe epigastric pain, retching without vomiting, inability to pass NG
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where are peptic ulcers most commonly located?
lesser curve of stomach or first part of duodenum
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what are the most common causes of peptic ulcer?
H.pylori NSAIDS chronic alcohol use gastric bypass severe burns head trauma zollinger ellison syndrome
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when should an urgent OGD be done in context of PUD?
New-onset dysphagia Aged >55 years with weight loss and either upper abdominal pain, reflux, or dyspepsia New onset dyspepsia not responding to PPI treatment
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which other investigations are required apart from OGD is required for PUD?
c-12 breath test, serum antibody to H pylori, stool antigen test
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how are peptic ulcers managed conservatively?
smoking cessation weight loss less alcohol less NSAIDS PPI or triple therapy if h,pylori
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why might surgery be required in PUD and why is it indicated?
only in emergencies when it perforates or if zollinger ellison syndrome in severe or relapsing - partial gastrectomy, selective vagotomy
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what are the risk fx for gastric cancer/
male h.pylori age smoking
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what are the clincial features of gastric cancer?
vague dyspepsia dysphagia early satiety vomit malaena non specific cancer sx epigastric mass troisier's sign - palpable left supraclavicular node hepatomegaly, ascites, jaundice
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which investigations for gastric cancer?
URGENT OGD for staging - CT TAP and staging laparascopy
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where should biopsies from a suspected gastric malignancy be sent?
histology CLO test - h.pylori HER2/neu protein expression - monocloncal therapies
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how is gastric cancer managed surgically>
proximal - total gastrectomy distal - subtotal gastrectomyy reconstructed with roue-en-Y
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what are some gastrectomy complications?
death anastamotic leak re operation dumping syndrome vit B12 defiency
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what are the main complications of gastric cancer
gastric oulet obstruction iron defiency anaemia perforation malnutrition
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define direct inguinal hernia
bowel enters through hesselbach's triangle medial to inferior epigastric vessels
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define indirect inguinal hernia
bowel enters the inguinal canal via deep inguinal ring. due to incomplete closure of processus vaginalis lateral to inferior epigastric vessels
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risk fx for inguinal hernia
Male gender Increasing age Raised intra-abdominal pressure, from chronic cough, heavy lifting, or chronic constipation High BMI
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what are the clinical fx of inguinal hernia
lump in groin..if reducible disappear when lying down mild discomfort if incarcerated - painful and non reducible possible bowel obstruction sx
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how do you examine any groin lump?
Cough impulse – remember that an irreducible hernia may not have a cough impulse Location – inguinal hernia appear superomedial to the pubic tubercle* (whilst femoral hernia appear inferolateral to the pubic tubercle) Reducible – On lying down or with gentle pressure If it enters the scrotum, can you get above it / is it separate from the testis
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how do you locate the deep inguinal ring?
midpoint of inguinal lig
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what are some differentials for groin lump?
femoral hernia, saphena varix, inguinal lymphadenopathy, lipoma, or groin abscess. If the mass extends into the scrotum, consider a hydrocoele, varicocoele, or a testicular malignancy.
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which investigations are required for groin lump
USS Ct if strangulation/obstruction
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how is an inguinal managed?
symptomatic - surgical strangulated (pain out of proportion or derranged UE) - surgery asx - maybe conservative
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how are inguinal hernias repaired surgically?
open repair(lichenstein) or laprascopic if primary = open mesh if bilateral or recurret or female/chronic pain = laprascopic
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what are the main complications following elective inguinal hernia repair?
haematoma, seroma, recurrence, chronic pain, damage to vas deferens or testicular vessels
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define femoral hernia
abdominal viscera or hernia pass through femoral ring and into potential space of femoral canal
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risk fx for femoral hernia
Female Pregnancy (higher incidence in multiparous women) Raised intra-abdominal pressure (e.g. heavy lifting, chronic constipation) Increasing age
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what are the clinical fx of femoral hernia?
small lump in groin usually p[resent as emergency as femoral canal narrow
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how do you differentiate between a femoral and inguinal hernia?
Femoral hernia – found infero-lateral to the pubic tubercle (and medial to the femoral pulse) Inguinal hernia – found supero-medial to the pubic tubercle A femoral hernia can roll up superiorly and in front of the inguinal ligament and are often misdiagnosed as inguinal
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how are femoral hernias managed?
all surgically within 2 weeks of presentation low approach = below inguinal lig high approach = easy access to small bowel ...reduce hernia and narrow femoral ring
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define epigastric hernia
through upper midline through fibres of linea alba secondary to raised intra abdo pressure usually middle aged men
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define paraumbilical hernia
through linea alba around umbilical region secondary to chronic raised intra abdo pressure contain usually pre peritoneal fat and bowel or in children - omphalocele or gastroschsiss
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define spigelian hernia
rare through semilunar line around level of arcuate line present as mass in lower lateral edge of rectus abdominus high risk of strangulation
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define obtruator hernia
hernia of pelvic floor - through obtruator foramen into obtruator canal more common in women due to wider pelvis usually elderly mass in upper medial thigh features of small bowel obstruction compression of obtruator nerve - postive howship-romberg sign
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define littre's hernia
very rare form of abdominal hernia, whereby there is herniation of a Meckel’s diverticulum. This most commonly occurs in the inguinal canal and many will become strangulated.
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define lumbar hernia
rare posterior hernias, that typically occur spontaneously or iatrogenically following surgery (classically following open renal surgery). They present as a posterior mass, often with associated back pain.
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define richter's hernia
only a partial herniation of bowel, where anti mesenteric border becomes stangulated so only one of lumen of bowel within hernia sac
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define richter's hernia
any hernia - only a partial herniation of bowel, where anti mesenteric border becomes stangulated so only one of lumen of bowel within hernia sac tender irreducible mass at orifice
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define gastroenteritis
inflammation of GI tract usually infective(viral)
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PC of gastroenteritis
diarrhoea, vomit,abdo pain night sweats, weight loss, dehydrated, pyrexia hx - bowel movements, affected family, recent travel, recent use of abx
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how do you differentiate between the causative organisms of gastroenteritis?
bacterial toxins - hours bacteria - weeks viruses - days parasites - months
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risk fx for gastroenteritis
Poor food preparation, especially in handling and cooking Immunocompromised Poor personal hygiene
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when may an investigations of gastroenteritis be required?
stool culture if blood or mucus in stool and if pt is immunocompromised or if severe or persitent
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how is gastroenteritis managed?
Rehydration, encouraging oral fluid intake where possible If severe dehydration or unable to tolerate oral fluid, the patient may need admission for intravenous fluid rehydration Education to prevent future episodes Exclusion from work is usually 48 hours from the last episode of vomiting or diarrhoea must notify!
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what are the viral causes of gastroenteritis?
Norovirus – single-stranded RNA virus (Fig. 1), the most common form of viral gastroenteritis in adults, presents with abdominal cramps, watery diarrhoea, and vomiting, usually lasting 1-3 days Rotavirus – double-stranded RNA virus, results in a severe diarrhoea among infants and young children, generally self-resolves in less than a week Adenovirus – double-stranded DNA virus, also a common cause of diarrhoea in children
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what are the bacterial causes of gastroenteritis?
Campylobacter –ingestion of affected chicken, eggs, or milk), can have a prodrome of fatigue, fever, or myalgia, followed by nausea, abdominal cramps, and diarrhoea Campylobacter infections can also result in reactive arthritis, Guillan Barre syndrome, haemolytic uraemic syndrome, and thrombotic thrombocytopaenic purpura E. Coli – contaminated foodstuffs (but can also spread from animals to human or from person to person contact); several forms of the bacteria exist, but Enterotoxigenic E. coli (ETEC) is the most common cause of Travellers’ diarrhoea E. coli serotype 0157:H7 is associated with causing haemorragic uraemic syndrome Salmonella – through undercooked poultry or raw eggs; results in fever, vomiting, abdominal cramps, and bloody diarrhoea Shigella – contaminated dairy products and water; presents with fever, abdominal pain, or bloody diarrhoea
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what are the bacterial toxins causing gastroenteritis?
symptoms tend to last less than 24 hours. Staphylococcus aureus – typically found in meat or dairy products, even re-heating of the cooked food does not destroy the exotoxin (even if the bacteria are destroyed) Bacillus cereus – usually found in reheated rice, known to cause rapid-onset vomiting and abdominal cramps Clostridium perfringes – typically acquired from re-heating meat dishes; causes diarrhoea yet vomiting is less common Vibrio cholera – acquired most commonly from contaminated water supplies and causes profound watery painless diarrhoea; an oral vaccine is available
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what are the parasitic causative organisms of gastroenteritis?
Cryptosporidium – protozoan that typically causes a self-limiting watery diarrhoea and abdominal cramps (can be life-threatening in those who are immunocompromised); diagnosis is made with stool culture for ova, cysts, and parasites. Entamoeba histolytica – anaerobic amoebozoan that becomes acquired from the ingestion of food or water contaminated with faeces (Fig. 3), presents with bloody diarrhoea, abdominal pain, and fever (can also result in liver abscess); stool culture for ova, cysts and parasites is required for diagnosis, recommended treatment is metronidazole or tinidazole Giardia intestinalis – parasite transmitted through direct contact or faeco-oral route, can cause either acute disease (diarrhoea, fever, fatigue, nausea, and bloating) or chronic disease (steatorrhoea, malabsorption, and weight loss); diagnosis made with stool culture for ova, cysts and parasites, recommended treatment is metronidazole or tinidazole Schistosoma – a fluke, acquired through contaminated water, with acute schistosomiasis developing about a month after the initial infection, presenting with fever, malaise, abdominal pain, bloody diarrhoea, and severe cases even leading to chronic liver disease; eosinophilia may be seen on full blood count and a stool culture for ova, cysts and parasites is required, with treatment via praziquantel
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what is the main causative organism for hospital acquired gastroenteritis?
c.diff...exotoxin A and B
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what is a complications of hospital acquired gastroenteritis?
toxic megacolon
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how is c.diff gastroenteritis diagnosed?
stool culture and c diff toxin testing...requires metronidazole
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what are the non infective causes of gastroenteritis?
Radiation colitis – inflammation of the gastrointestinal tract secondary to radiation therapy Inflammatory bowel disease, such as Crohn’s Disease or Ulcerative Colitis Microscopic colitis – a condition where the colon is macroscopically normal on endoscopy however biopsy demonstrates an increase in the number of inflammatory cells present Chronic ischaemic colitis – caused by a compromise in blood supply to the colon, most commonly affecting the watershed area around the splenic flexure. Diagnosis is confirmed by endoscopy where one might observe ‘blue swollen mucosa’
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what is angiodysplasia?
formation of arteriovenous malformations very common - rectal bleeding >60
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what is the pathophysiology of angiodysplasia?
Acquired angiodysplasia – begins as reduced submucosal venous drainage in the colon due to chronic and intermittent contraction of the colon, giving rise to dilated and tortuous veins. This results in the loss of pre-capillary sphincter competency and in turn causes the formation of small arterio-venous communications characterized by a small tuft of dilated vessels. Congenital angiodysplasia – included causes such as hereditary haemorrhagic telangectasia (Rendu-Osler-Weber syndrome)
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what are the clinical features of angiodysplasia?
rectal bleeding and anaemia either asx, painless occult PR bleeding, acute haemorrhage haematemesis or malaena
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what are the ddx for angiodysplasia?
oesophageal varices, gi malignancies, diverticular disease
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which investigations are required for angiodysplasia?
FBC, UE, LFTS, clotting, group and save or crossmatch upper gi for malignancy wireless capsule endoscopy - small bowel bleeds mesenteric angiograpjy - overt bleed
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how is angiodysplasia managed?
conservatively - bed rest and IV fluid, tranxamic acid endoscopy - subjecting vessel to electric current and argon mesenteric angiography - super selective catheterisation and embolisation of vessel surgery - resection and anastomosis of affected bowel
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what are the risk fx with poor outcome for angiodysplasia?
age,liver disease, hypovolaemic shock, current inpatients
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what are the indications of bowel surgery for angiodysplasia?
Continuation of severe bleeding despite angiographic and endoscopic management (or such therapies are unavailable) Severe acute life-threatening GI bleeding Multiple angiodysplastic lesions that cannot be treated medically
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how common are small bowel tumours?
rare <5%
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where is the most common location for small bowel tumours?
duodenum jejenum ileum
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what are the histology of small bowel tumours>
Benign tumours – typically adenomas, subclassified as simple villous, tubular, or Brunner’s gland adenomas; less common types are leiomyomas, lipomas, and desmoid tumours Malignant tumours – most common types are either adenocarcinomas or neuroendocrine tumours (40% each*); less common types are stromal tumours, sarcomas, and lymphomas
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what is the pathophysiology of small bowel tumours?
re-existing adenomas through a sequential accumulation of genetic abnormalities (in a model similar to that described for the pathogenesis of colorectal cancer), which can occur over several years. The tumour suppressor gene p53, which maintains DNA integrity, and the oncogene KRAS, which normally functions in cellular signalling and proliferation, have been implicated in over 50% of small bowel adenocarcinoma cases.
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what are the risk fx for small bowel tumours?
age, crohns, coeliac, genetic (familial adenomatous polyposis) smoking, obesity, low fibre, high red meat, alcohol
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what are the clinical fx for small bowel cancer?
usually asx small bowel obstruction as increase in size PR bleeding abdo mass, cachexia, jaundice, hepatomegaly, ascites
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which investigations are required for small bowel tumours?
elevated CEA LIVER metastasis - 5-HIAA upper GI endoscopy MRI enterography bowel obstruction - CT
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how is small bowel cancer managed?
local small bowel adenocarcinomas - surgical resection duodenal tumours - pancreaticoduodenectomy lymph nodes - adjuvant chemo mets - chemo
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define neuroendocrine tumour
originating from neuroendocrine cells in the gastrointestinal tract or the pancreas*, all of which have malignant potential; pancreatic neuroendocrine tumours are discussed further here The incidence of GEP-NETs is between 2-3 per 100 000 persons per year, with slightly higher rates in women, and rates have been increasing in recent years. The majority of GEP-NETs are located in the small intestine, the remainder either in the rectum or the stomach.
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define neuroendocrine tumour
originating from neuroendocrine cells in the gastrointestinal tract or the pancreas*, all of which have malignant potential; pancreatic neuroendocrine tumours are discussed further here The incidence of GEP-NETs is between 2-3 per 100 000 persons per year, with slightly higher rates in women, and rates have been increasing in recent years. The majority of GEP-NETs are located in the small intestine, the remainder either in the rectum or the stomach.
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what are the risk fx of neuroendocrine tumour?
complex familial endocrine cancer syndromes such as MEN1, MEN2, neurofibromatosis type 1 (NF1), Von Hippel Lindau (VHL), and Carney complex, however the majority of NETs occur are sporadic. Other risk factors include female gender and family history of NETs.
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what are the clinical fx of neuroendorcrine tumour?
non-functioning tumours (the majority), which have no hormone-related clinical features, or functioning tumours, which cause symptoms due to peptide and hormone release. All GEP-NETs can present with non-specific symptoms, such as vague abdominal pain, nausea and vomiting, and abdominal distension. In less common cases, they may present with features of bowel obstruction (or appendicitis in appendiceal GEP-NETs), requiring urgent intervention
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which investigations are required for neuroendocrine tumours?
CgA - high in functional and non functional PP high when CgA and CgB are normal urinary 5-HIAA CT enteroclysis endoscopy whole body somatostatin receptor schintigraphy
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how is neuroendocrine tumours managed?
. Surgery is the only curative treatment for GEP-NETs*, however nodal or liver metastases are found at presentation in 40–70% of patients. Well-differentiated GEP-NETs are managed according to site, staging, and functionality. Localised disease should be resected; any liver metastases present should also be resected where feasible, along with the primary tumour, as this has been shown to improve survival rates. Poorly-differentiated GEP-NETs have a poor prognosis; if the disease is localised, then treatment is often surgical resection followed by chemotherapy, whilst in metastatic disease, palliative chemotherapy alone is typically advised. surgery -
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surgery for neuroendocrine tumour
Gastric NETs management grade, as the lower subtypes often have a very low metastatic potential, therefore can usually be treated with endoscopic resection and annual surveillance. However, the more aggressive lesions should be treated more aggressively, requiring gastrectomy with regional lymph node clearance. Small intestinal NETs are almost always malignant. Resection of the tumour with mesenteric lymph node clearance is nearly always performed, regardless of the presence of liver metastases. Appendiceal NETs are often identified incidentally following appendicectomy. A completion right hemicolectomy will be required for tumours >2cm in size, with a serosal breach, cellular atypia, invasion of mesoappendix (by more than 3 mm), or involvement of the base of the appendix Colonic NETs have the worst prognosis of any gastrointestinal NET, with their treatment often requiring a segmental colectomy with regional lymph node clearance. Rectal NETs have a more benign character, with smaller tumours treated with endoscopic resection and larger tumours requiring either AP resection or low anterior resection.
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prognosis for neuroendocrine tumour
slow growing rectal - highest sruvical rates
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what is the pathophysiology behind an acute appendicitis?
caused by direct luminal obstruction, usually secondary to a faecolith (Fig. 1) or lymphoid hyperplasia, impacted stool or, rarely, an appendiceal or caecal tumour. When obstructed, commensal bacteria in the appendix can multiply, resulting in acute inflammation. Reduced venous drainage and localised inflammation can result in increased pressure within the appendix, in turn can result in ischaemia. If left untreated, ischaemia within the appendiceal wall can result in necrosis, which in turn can cause the appendix to perforate.
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risk fx for appendicitis
family history caucasians summer
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sx of appendicitis
abdo pain - peri umbilical from visceral perioteneum inflammation and migrates to RIF when parietal peritoneum is inflammed vomit anorexia nasua diarrhoea constipation rebound tenderness and percussion pain over mcburneys point appendiceal abscess may be able to be palpated tachycardic and hypotensive guarding if peritonitic
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which clinical signs can be illicited in an acute appendicitis?
Rovsing’s sign: RIF fossa pain on palpation of the LIF Psoas sign: RIF pain with extension of the right hip Specifically suggests an inflamed appendix abutting psoas major muscle in a retrocaecal position
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how might an acute appendicitis present in children?
diarrhoea, urinary symptoms, or even left sided pain
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ddx for appendicitis
Gynaecological: ovarian cyst rupture, ectopic pregnancy, pelvic inflammatory disease Renal: ureteric stones, urinary tract infection, pyelonephritis Gastrointestinal: inflammatory bowel disease, Meckel’s diverticulum, or diverticular disease* Urological: testicular torsion, epididymo-orchitis Specifically in children, differentials to consider include acute mesenteric adenitis, gastroenteritis, constipation, intussusception, or urinary tract infection.
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which investigations are required for an eppendicitis?
urinalysis preg test FBC, CRP, UE, seum beta HCG men - CT, women -USS then CT
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how is an appendictis managed?
laprascopic appendicectomy abx appendix then sent to histology for malignancy
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give some complications of appendicitis
Perforation, if left untreated the appendix can perforate and cause peritoneal contamination This is particular note in children who may have a delayed presentation Surgical site infection Rates vary depending on simple or complicated appendicitis (ranging 3.3-10.3 %) Appendix mass, where omentum and small bowel adhere to the appendix Pelvic abscess Presents as fever with a palpable RIF mass, can be confirmed CT scan for confirmation; management is usually with antibiotics and percutaneous drainage of abscess
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how common colorectal cancer
second highest mortality 4th most common 20 yr -40 yrs old
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how do colorectal cancers develop?
via a progression of normal mucosa to colonic adenoma (colorectal ‘polyps’) to invasive adenocarcinoma (termed the “adenoma-carcinoma sequence”). Adenomas may be present for 10 years or more before becoming malignant; progression to adenocarcinoma
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which genetic mutations are mostly associated with colorectal cancer?
APC, HNPCC
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what are the risk fx of colorectal cancer?
increasing age,male, family hx, IBD, low fibre diet, high processed meat, smoking, excess alcohol
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what are the clinical features of colorectal cancer?
change in bowel habit rectal bleeding weight loss abdo pain iron def anaemia vary on position -Right-sided colon cancers – abdominal pain, iron-deficiency anaemia, palpable mass in right iliac fossa, often present late Left-sided colon cancers – rectal bleeding, change in bowel habit, tenesmus, palpable mass in left iliac fossa or on PR exam
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what's the criteria for referralof urgent investigations of suspected bowel cancer?
≥40yrs with unexplained weight loss and abdominal pain ≥50yrs with unexplained rectal bleeding ≥60yrs with iron‑deficiency anaemia or change in bowel habit Positive occult blood screening test
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ddx for colorectal cancer
IBD, haemorrhoids
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how does colorectal cancer screening work?
every 2 yrs for men and women 60-75yrs FIT test if positive - colonoscopy
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which investigations are required for colorectal cancer?
FBC - microcytic anaemia LFT clotting CEA - monitor disease progression colonoscopy with biopsy staging process - CT TAP, MRI rectum, endo anal USS
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how is colorectal cancer staged?
dukes Stage Description 5 Year Survival A Confined beneath the muscularis propria 90% B Extension through the muscularis propria 65% C Involvement of regional lymph nodes 30% D Distant metastasis <10%
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how is colorectal managed
MDT asurgery and chemo and radio - chemotherapy regime for patients with metastatic colorectal cancer is FOLFOX, comprised of Folinic acid, Fluorouracil (5-FU), and Oxaliplatin regional colectomy radio - rectal cancer
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right hemicolectomy
The surgical approach for caecal tumours or ascending colon tumours, with the extended option performed for any transverse colon tumours. During the procedure the ileocolic, right colic, and right branch of the middle colic vessels (branches of the SMA) are divided and removed with their mesenteries
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left hemicolectomy
The surgical approach for descending colon tumours. Similar to the right hemicolectomy, the left branch of the middle colic vessels (branch of SMA/SMV), the inferior mesenteric vein, and the left colic vessels (branches of the IMA/IMV) are divided and removed with their mesenteries
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sigmoidectomy
The surgical approach for sigmoid colon tumours. In this instance, the IMA is fully dissected out with the tumour in order to ensure adequate margins are obtained.
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anterior resection
The surgical approach for high rectal tumours, typically if >5cm from the anus. This approach is favoured as leaves the rectal sphincter intact if an anastomosis is performed (unlike AP resections). Often a defunctioning loop ileostomy is performed to protect the anastomosis and reduce complications in the event of an anastomotic leak, which can then be reversed electively four to six months later
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AP resection
The surgical approach for low rectal tumours, typically <5cm from the anus. This technique involves excision of the distal colon, rectum and anal sphincters, resulting in a permanent colostomy
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hartmanns procedure
used in emergency bowel surgery, such as bowel obstruction or perforation. This involves a complete resection of the recto-sigmoid colon with the formation of an end colostomy and the closure of the rectal stump
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define diverticulitis/diverticular disease
Diverticulosis – the presence of diverticula (asymptomatic, incidental on imaging) Diverticular disease – symptoms arising from the diverticula Diverticulitis – inflammation of the diverticula Diverticular bleed – where the diverticulum erodes into a vessel and causes a large volume painless bleed
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what is the pathophysiology behind diverticular disease?
aging bowel becomes weakened over time, movement fo stool causes increased intraluminal pressure...outpouchings of musosa through weaker areas of bowel wall...bactera can overgrow...inflammation which can perforate..peritonitis and death fistula can form - colovesicular or colovaginal
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simple v chronic diverticulitis
complicated - abscess or free perforation simple - inflammation without these features
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risk fx for diverticular disease
age, low dietary fibre intake, obesity, smoking, family history, and NSAID use.
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what are the clinical fx of diverticulosis etc?
diverticulosis - asx diverticular disease - intermittent lower abdo pain, relieved by defecation, altered bowel habit, nausea, flatulence acute diverticulitis - acute abdo pain LIF, tenderness, decreased appetite, pyrexia, nausea perforated - peritonism
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which investigations are required for diverticulitis?
FBC, CRP, UE, faecal calprotectin group and save venous blood gas urine dipstick CT abdo plevis - thicekning colonic wall, pericolonic fat stranding, abscesses, localised air bubbles, free air flexy sig if uncomplicated CT colonoscopy if complicated
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how is diverticulitis staged?
hinchey classification - CT findings Stage 1 Phlegmon (1a) or diverticulitis with pericolic or mesenteric abscess (1b) Stage 2 Diverticulitis with walled off pelvic abscess Stage 3 Diverticulitis with generalised purulent peritonitis Stage 4 Diverticulitis with generalised faecal peritonitis
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how is diverticular disease managed?
uncomplicated - analgesia, fluid, outpatient colonoscopy to exclude malignancies diverticular bleeds - as above, blood products too if not respond - embolisation or surgical resection acute diverticulitis - abx, IV fluids, analgesia, surgery - if perforated with faecal peironitis/sepsis ...hartmann's
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give some complications of diverticulitis
recurrence, stricture causing large bowel obstruction or fistula formation (colovesical - recurrent UTI, pneumoturia - gas bubbles in urine, colovaginal - vaginal discharge)
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crohns age distribution
bimodal
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define crohns disease
affects any part of GI tract - distal ileum or proximal colon familial link smoking increases risk transmural inflammation deep ulcers and fissures skip lesions non caseating granulomatous fistula can form - usually perianal
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differences between crohns and uc
Ulcerative Colitis Crohn’s Disease Site Involvement Large bowel Entire GI tract Inflammation Mucosa only Transmural Microscopic Changes Crypt abscess formation Reduced goblet cells Non-granulomatous Granulomatous (non-caseating) Macroscopic Changes Continuous inflammation (proximal from rectum) Pseudopolyps and ulcers may form vs Discontinuous inflammation (‘skip lesions’)Fissures and deep ulcers (‘cobblestone appearance’) Fistula formation
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risk fx of crohns
family history smoking
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what are the clinical features of crohns disease
colicky pain, diarrhoea, can contain blood or mucus, malaise, anorexia, low grade fever, perianal disease like abscess, oral apthous ulcers
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what are the extra intestinal mainfestations of crohns?
Musculoskeletal, such as Enteropathic arthritis (typically affecting sacroiliac and other large joints), nail clubbing, or with metabolic bone disease (secondary to malabsorption) Skin, either as erythema nodosum (tender red/purple subcutaneous nodules, typically on the shins or pyoderma gangrenosum (erythematous papules/pustules that develop into deep ulcers Eyes – Episcleritis, anterior uvetitis, or iritis Hepatobiliary – Primary sclerosing cholangitis (more associated with UC), cholangiocarcinoma (due to association with primary sclerosing cholangitis), or gallstones Renal – Renal stones
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which investgiations are required for crohns disease?
routine bloods - anaemia, low albumen, evidence of inflammation faecal calprotectin test stool sample for infective causes colonoscopy with biopsies CT abdo pelvis - bowel obstruction, perforation, intra abdominal collections, MRI - fistula, peri anal disease or EUA for perianal
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how is crohns disease managed
referred to gastroenterologist loperamide - in acute attacks inducing remission - fluids, heparin and anti-embolic stockings (due to the prothrombotic state of IBD flares). corticosteroid therapy, immunosuppresive agents, such as mesalazine or azathioprine, or biological agents, such as infliximab or adalimumab maintaining remission - azathioprine, colonoscopic surveillance as risk of malignancy, enteral nutritional support surgical - Ileocaecal resection (removal of terminal ileum and caecum with primary anastomosis) Small bowel resection or large bowel resection Surgery for peri-anal disease (e.g. abscess drainage, seton insertion, or laying open of fistulae) Stricturoplasty (division of a stricture that is causing bowel obstruction)
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give some complications of crohns disease
Fistula, including enterovesical, enterocutaneous, or rectovaginal fistula Stricture formation Recurrent perianal fistulae GI malignancy
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give some extraintestinal complications of crohns
Malabsorption, including growth delay in children Osteoporosis, secondary to malabsorption or long-term steroid use Increased risk of gallstones, due to reduced reabsorption of bile salts at the terminal ileum Increased risk of renal stones – Due to malabsorption of fats in the small bowel which causes calcium to remain in the lumen; oxalate is then absorbed freely (as normally bound to calcium and excreted in stool), resulting in hyperoxaluria and formation of oxalate stones in the renal trac
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distibution of UC
bimodal
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aetiology of UC
unknown
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pathophysiology behind UC
diffuse continual mucosal inflammation of large bowel beginning in rectum spreading proxiamlly but only to large bowel non granuloamatous inflammation, crypt abscesses, goblet cell hypoplasia, psuedopolyps
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what are the clinical features of UC?
blood diarrhoea proctitis - inflammation confined to rectum PR bleeding and mucus discharge increased frequency and urgency of defecation and tenesmus dehydration electrolyte imbalance malaise anorexia low grade pyrexia if severe abdo pain - toxic megacolon or colonic perforation
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ddx what are some extra intestinal manifestations of UC?
Musculoskeletal – enteropathic arthritis (typically affecting sacroiliac and other large joints) or nail clubbing Skin – Erythema nodosum (tender red/purple subcutaneous nodules, typically on the shins, Fig. 2) Eyes – Episcleritis, anterior uveitis, or iritis Hepatobiliary – Primary sclerosing cholangitis* (chronic inflammation and fibrosis of the bile ducts)
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ddx for UC
crohns schistosomiasis mesenrteric ischaemia radiation colitis IBS coeliac
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which investigations are required for UC?
FBC, UE, CRP, LFT, clotting - anaemia, low albumin, inflammation faecal calprotectin - raised in IBD, unchanged in IBS stool sample colonoscopy with biopsy plain film radiographs or CT for toxic megacolon and bowel perforation, mural thickening, thumbprinting, lead pipe colon in chronic cases
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how is UC managed?
sameas crohns medical management to induce remission in UC typically requires use of intravenous corticosteroid therapy and immunosuppresive agents, such as ciclosporin or 5-ASA suppositories. Biological agents, such as infliximab, can be trialled as rescue therapy if then needed. surgery - segemenratl bowel resection, for elective - total proctocolectomy is curative
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give some complications of UC
toxic megacolon, colorectal carcinoma, osteoporosis, pouchitis
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define pseudo obstruction
dilation of colon due to an adynamic bowel in the abasence of mechanical obstruction affects mainly caecum and ascending colon due to interruption of the autonomic nervous supply to the bowel leading to increased risk of toxic megacolon, bowel ischameia and perforation
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give some causes of pseudo obstruction
Electrolyte imbalance or endocrine disorders Including hypercalcaemia, hypothyroidism, or hypomagnesaemia Medication Including opioids, calcium channel blockers, or anti-depressants Recent surgery, severe illness, or trauma Includes cardiac ischaemia Neurological disease Includes Parkinson’s disease, Multiple Sclerosis, and Hirschsprung’s disease
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what are the clinical fx of pseudo obstruction?
abdo pain, distention, constipation, vomit, typanic on exam, non tender
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what are the ddx for pseudo-obstruction?
Mechanical obstruction Paralytic ileus Toxic megacolon
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which investigations are required for pseudo-obstruction?
FBC, UE, calcium,magnesium,TFTs, plain film radiographs - bowel distention abdo pelvis CT with IV - dilation of colon
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how is pseudoobstruction managed?
NBM IV fluids NG endoscopic decompression nutrition if perforates or ischaemia - segmental resection or caecostomy or ileostomy
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risk fx of volvulus
Increasing age Neuropsychiatric disorders Resident in a nursing home Chronic constipation or laxative use Male gender Previous abdominal operation
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what are teh clinical fx of volvulus?
bowel obstruction - colicky pain, distention, absolute constripation, rapid onset, tympanic to percussion
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what are the ddx of volvvulus?
severe constipation, pseudo-obstruction, sigmoid diverticular disease
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which investigations are required for volvulus?
routine bloods - calcium, TFT to exclude pseudo-obstruction CT abdo pelvis - very dilated sigmoid colon with a whirl sign from twisting mesentery abdo x ray - coffe bean from left iliac
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how is a volvulus managed?
fluid resuscitation decompression by signmoidoscope and insertion of flatus tube through rectum surgery - laparotomy for hartmanns
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what are the indications for surgery of a volvulus?
Colonic ischaemia or perforation Repeated failed attempts at decompression Necrotic bowel noted at endoscopy
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what are the main complications of a sigmoid volvulus?
bowel ischaemia and perforation risk of recurrence
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what is the age distribution of a caecal volvulus?
bimodal younger -intestinal malformations or excessive exercise which predisposes them older - chronic constripation, distal obstruction, dementia
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how does a caecal volvulus appear on CT?
swirl in RIF
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how is a caecal volvulus managed?
lapratomy and ileocaecal resection
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define haemorrhoids
abnormal swelling or enlargement of the anal vascular cushions.
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how are haemorrhoids classified?
1st Degree Remain in the rectum 2nd Degree Prolapse through the anus on defecation but spontaneously reduce 3rd Degree Prolapse through the anus on defecation but require digital reduction 4th Degree Remain persistently prolapsed
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what are the risk fx of haemorroids?
excessive straining, increased age, raised intra abdo pressure
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what are the clinical fx of haemorrhoids?
painless bright red rectal bleeding pruritus rectal fullness soiling can thrombose which is painful - purple oedematous tense and tender peianal mass
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what are the ddx for haemorrhoids?
malignancy, IBD, diverticular disease, fissure in ano, perianal abscess, fistula in ano
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which investigations are required for haemorrhoids?
proctoscopy fbc - prolonged bleeding colonosocpy - other anorectal pathology
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how are haemorrhoids managed?
usually conservatively - more fibre, fluid, laxative, topical lignocaine, oral opioids avoided, 1st and 2nd degree - rubber band ligation surgery - haemorrhoidal artery ligation - blood supply identified through doppler and tiesdoff or haemorrhoidectomy but leave internal sphincter muscle...can result in incontinence
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define pilonidal sinus disease
disease of the inter-gluteal region*, characterised by the formation of a sinus in the cleft of the buttocks. It most commonly affects males aged 16-30 years . *The term pilonidal is derived from the Latin pilus (hair) and nidus (nest).
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what is the pathophysiology of pinodial sinus disease?
starts from hair follicle which extends inwards forming a pit...foreign body reaction leads to formation of cavity
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what are the risk factorsfor pilonidal sinus disease?
caucasian male coarse dark hair sit for long periods increased sweating buttock friction obesity poor hygeien local trauma
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what are the clinical fx for pilionidal sinus disease?
discharging and intermittently painful sinus in sacrococcygeal region ...can form an abscess does nto communicate with anal canal - rigid sigmoidoscopy or MRI to compare with fistula
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how is pilonidal sinus disease managed?
shaving affected region and pluck sinus washed out abx in septic/abscess surgery - incision and drainage if chronic - removal of pinonidal sinus tract
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define perianal fistula
an abnormal connection between the anal canal and the perianal skin.abscess becomes fistula
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how are perianal fistulas clasified?
Park’s Classification System divides anal fistulae into four distinct types; inter-sphincteric fistula (most common), trans-sphincteric fistula, supra-sphincteric fistula (least common), and extra-sphincteric fistula
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what are teh causes of perianal fistula?
from abscess - Inflammatory bowel disease, mainly perianal Crohn’s Disease Systemic diseases, typically Diabetes Mellitus History of trauma to the anal region Previous radiation therapy to the anal region
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what are the clinical fx of fistula?
recurrnet perianal abscess, intermittent or continuous discharge onto perineum - mucus, blood, pus, faeces examination - an external opening on the perineum DRE - fibrous tract felt underneath skin
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define goodsall rule
predicts trajectory of fistula tract depending on location of external opening External opening posterior to the transverse anal line – fistula tract will follow a curved course to the posterior midline External opening anterior to the transverse anal line – fistula tract will follow a straight radial course to the dentate line
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which investigations are required for perianal fistula?
MRI
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how is a perianal fistula managed?
For those due to perianal Crohn’s disease (following drainage of any perianal abscess present), medical management of the Crohn’s disease is often started first prior to further surgical intervention surgery - fistulotomy -lays tract open and cuts skin and tissues, placement of a seton - bring together and closes the tract...if low track coruse - faceal incontinence is rarely impaired versus high track
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define anorectal abscess
collection of pus in the anal or rectal region. They are more common in men than in women and have high rates of recurrence. One third of patients with an anorectal abscess have an associated perianal fistula at the time of presentation.
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what is the pathophysiology behind anorectal abscess?
plugging of the anal ducts which drain the anal glands in the anal wall....fluid stasis and infection usually due to e.coli or enterococcus
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how can anorectal abscesses be categroised?
(1) Perianal* (2) Ischiorectal (3) Intersphincteric (4) Supralevator
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what are the clinical fx of anorectal abscesses?
evere pain in the perianal region, worse with direct pressure (i.e. when sat down), alongside potential perianal discharge or bleeding. Severe abscesses may present with systemic features* such as fever or rigors, general malaise, or clinical features of sepsis. On examination, there will be a erythematous, fluctuant, tender perianal mass (Fig. 1), which may be discharging pus or have surrounding erythema and induration. Deeper abscesses may not have any obvious external signs, however produce severe tenderness on PR examination.
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which investigations are required for perianal abscesses?
FBC, UE, clotting, Group and save for surgery HbA1C if no fistula to check if diabetic if atypical or complex - MRI
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how are perianal abscesses managed?
abx analgesia EUA rectum and incision and drainage and left heal by secondary intention intra op proctoosocpy to check for fistula and then inserted seton post op abx
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define anal fissure
tear in the mucosal lining of the anal canal, most commonly due to trauma from defecation of hard stool
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how can anal fissures be classified?
Acute – present for <6 weeks Chronic – present for >6 weeks or primary versus secondary from IBD
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what are the risk fx of an anal fissure?
constipation dehydration IBC chronic diarrhoea
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what are the clinical fx of fissure?
intense pain post-defecation Pain can be far out of proportion to the size of the fissure. Other associated symptoms may include bleeding (commonly bright red blood on wiping) or itching, both typically post-defecation fissure scna be visible most common - usually in posterior midline dre - exmaination under anaesteheisa or prcotsopcy but may be too painful
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how is anal fissure managed?
reduce risk fx analgesua fibre and fluid intake increase stool softener laxative topical lidocaine GTN cream if chronic = botox injections or lateral sphincterotomy
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define rectal prolapse
protrusion of mucosal or full-thickness layer of rectal tissue out of the anus. - mianly older women
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give 2 types of rectal prolapse
Partial thickness – the rectal mucosa protrudes out of the anus Full thickness – the rectal wall protrudes out the anus
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what are the pathophysiologies behind anal; prolapse
full prolapse suggest that is a form of sliding hernia, through a defect of the fascia of the pelvic region. This may be caused by chronic straining secondary to constipation, a chronic cough, or from multiple vaginal deliveries. In contrast, partial thickness prolapses are associated with the loosening and stretching of the connective tissue that attaches the rectal mucosa to the remainder of the rectal wall. This often occurs in conjunction with long standing haemorrhoidal disease.
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what are the risk fx for rectal prolapse?
increasing age, female gender, multiple deliveries, straining, anorexia, and previous traumatic vaginal delivery
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what are the clinical fx of rectal prolpase?
rectal mucus discharge, faecal incontinence, per rectum bleeding, or with visible ulceration. Full thickness prolapses will begin internally and thus can initially present with a sensation of rectal fullness, tenesmus, or repeated defecation. prolpase seen when straining For a suspected internal prolapse, defecating proctography and examination under anaesthesia
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how is an anal prolpase managed?
dietary fibre, fluid increase banded in clinic surgery - abdo and perineal approach
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what are the types of anal cancer?
squamous cell - above dentate line - majority (can be anal intraepithelial neoplasia before and is strongly linked to HPV) adenocarcinoma melanomas and anal skin cancers
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what are the risk fx for anal cancer?
HPV infection (accounts for 80-90% of cases, especially HPV-16 and HPV-18), HIV infection, increasing age, smoking, immunosuppression, or Crohn’s disease.
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what are the clinical fx of anal cancer?
rectal pain and bleeding anal discharge pruritus palpable mass infection and fistula faecal incontinence if sphinctersinvolved ulceration or wart like lesions lymphadenopathy
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where does lymph drain in the rectal region?
*Lymph from the area below the dentate line drains to the superficial inguinal nodes, whereas the anal canal and rectum above the dentate line drain into the mesorectal, para-aortic, and paravertebral nodes.
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which investigations are required for anal cancer?
proctosocopy EUA smear test - CIN or VIN HIV test USS guided fine needle aspiration CT TAP MRI pelvishow
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how is an anal cancer managed?
MDT chemo-radiation via external beam surgical excision if advanced - AP resection
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what is the complication of tx for anal cancer?
Chemoradiation-related pelvic toxicity is the most common short term complication, which can present with dermatitis, diarrhoea, proctitis, and/or cystitis. Longer term, patients may develop fertility issues, faecal incontinence, vaginal dryness, erectile dysfunction, and rectovaginal fistula.
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what is the prognosis of anal cancer?
stage versus 5 yr survival rate I 69.5 II 61.8 IIIa 45.6 IIIb 39.6 IV 15.3
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what is the biggest risk factor for anal cancer?
HPV infection