General Surgery (colorectal) Flashcards

1
Q

What are the causes of pancreatitis?

A

Gallstones
Alcohol
Steroids

Other:
- trauma, mumps, SLE, ERCP, hypothermia, hypercalcaemia

Drugs:
- azathioprine and mesalazine, NSAIDs, diuretics, sodium valproate

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2
Q

Brief pathophysiology of pancreatitis

A

duct obstruction leads to ischaemia and acinar cell injury

  • lipase released: fat necrosis with fatty acids binding calcium leading to hypocalcaemia
  • islet cells damaged: hyperglycaemia
  • protease and elastase released: haemorrhage

All leading to infection and inflammation

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3
Q

Aside from pancreatitis, when else would amylase be raised?

A
Ectopic pregnancy 
Renal failure
DKA
cholecystitis 
mesenteric ischaemia
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4
Q

Why is serum lipase not accurate in diagnosing pancreatitis?

A

It takes 8 hours after symptom onset to rise

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5
Q

If you were to do an AXR or CXR in pancreatitis, what might it show?

A

CXR: pneumoperitoneum or pleural effusion
AXR: sentinel loop sign (dilated proximal bowl)

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6
Q

What are the signs and symptoms of pancreatitis?

A

Epigastric pain radiating to the back
Guarding
Nausea and vomiting
Tetany (hypocalcaemia)

Tachycardic and hypotensive
Cullens: peri-umbilical brusing
Grey-turners: flank brusing
Left sided pleural effusion

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7
Q

What system would you use to calculate the severity/prognosis? What are some markers used in this score?

A

Glasgow scoring system
Low sats
>55

Raised neutrophils
Raised Urea
Raised LDH
Raised glucose

Hypoalbuminaemia
Hypocalcaemia

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8
Q

What is the management of pancreatitis?

A

IV Fluids
Analgesia
Antiemetics
Monitor Blood Glucose

Analgesia

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9
Q

What are some complications of pancreatitis?

A
Infective necrosis
Abscess
Pseudocyst 
Chronic pancreatitis 
DIC
ARDS and pleural effusions
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10
Q

What is the difference between acute and chronic pancreatitis? Therefore, how does chronic pancreatitis present?

A

In chronic pancreatitis it is the secretory function of the pancreas that is damaged
Diabetes
Steatorrhea
+ pain after eating

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11
Q

What are the causes of chronic pancreatitis?

A

Alcohol
Cystic fibrosis
Duct obstruction with tumour or stones

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12
Q

How should you investigate chronic pancreatitis? What is seen?

A

CT

Shows pancreatic calcifications

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13
Q

How is chronic pancreatitis managed?

A

Fat soluble vitamins
Pancreatic enzymes
Analgesia

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14
Q

Where are pancreatic pseudocysts most commonly located?

A

Lesser sac

Gastro-epiploic foramen

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15
Q

How do pancreatic pseudocysts present?

A

Biliary or gastric outlet obstruction

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16
Q

When and how does post-op ileus present?

A

Few days post-op

!!Hypovolaemia and low electrolytes despite positive fluid balance!!

Distension
N&V
Absolute constipation

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17
Q

What is third spacing?

How is it managed?

A

obstruction = proximal bowel hugely dilates = increased peristalsis = electrolyte rich secretions move from vascular space to bowel

Fluid resus

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18
Q

How does bowel obstruction present?

A

Distension + absolute constipation + vomiting + pain + empty rectum

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19
Q

What measurements constitute enlarged small bowel, large bowel and caecum?

A

small >3cm
large >6cm
caecum >9cm

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20
Q

What causes large bowel obstruction?

A

Colorectal cancer
Diverticulitis
Volvulus
IBD

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21
Q

What causes small bowel obstruction?

A

Hernia
Adhesions
Tumours, peritoneal metastasis, lymphomas

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22
Q

Compare what you’d hear on auscultation of large and small bowel obstruction

A

Large: loud but normal pitch
Small: high pitch tinkling

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23
Q

Percussion of a small bowel obstruction sounds like what?

A

Tympanic

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24
Q

How is bowel obstruction managed?

A

Fluid resuscitation

NG tube to decompress

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25
Q

A competent ileo-caecal valve leads to what?

A

Worsening bowel obstruction as material continues to pass in to the caecum leading to it rupturing

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26
Q

Where are peptic ulcers most commonly found?

A

lesser curve and antrum of the stomach

anterior proximal duodenum

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27
Q

What are the risk factors for developing peptic ulcers?

A
H-pylori infection
NSAIDs
Smoking
Alcohol
Zollinger Ellison
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28
Q

Briefly, how does H-pylori lead to ulcers?

A
  • reduced bicarbonate production
  • reduced mucous production
  • increased histamine leading to excessive acid
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29
Q

What is H-pylori?

A

spiral shaped gram -ve bacteria

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30
Q

How does peptic ulcers present in general?

What features point towards the ulcer being in the stomach vs duodenum?

A

Epigastric pain
Weight loss due to pain and early satiety

stomach: pain just before and whilst eating
duodenal: improved by eating then pain worse hours after

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31
Q

How would you investigate peptic ulcer disease?

A

urease breath test
stool antigen test
+/- endoscopy and biopsy

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32
Q

What does H-pylori eradication involve?

A

Omeprazole
Amoxicillin
Metronidazole or clarithromycin

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33
Q

What are the complications of peptic ulcer disease?

A
perforation leading to peritonitis 
anaemia 
malignancy
haemorrhage 
- stomach = left gastric
- duodenum = gastroduodenal
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34
Q

How is haemorrhage resulting from peptic ulcer erosion managed?

A

inject adrenaline
cauterize
omeprazole

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35
Q

What can cause peritonitis?

A

GI tract perforation
Spontaneous bacteria peritonitis (seen in ascites)
Peritoneal dialysis
Surgical complication

Non-infectious eg with SLE

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36
Q

How does peritonitis present?

A

acute abdominal pain
washboard rigidity
fever
shock

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37
Q

What are the complications of peritonitis?

A

abscess formation
sepsis
fluid and electrolyte disturbances
breathing difficulties if diaphragm irritated or under pressure in abdomen distension

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38
Q

What nerves cause the classic generalised then localising to RIF pain seen in appendicitis?

A

General: visceral splanchnic
Localised: peritoneal

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39
Q

What are some examination findings in appendicitis?

A
RIF rebound tenderness 
Guarding 
Rosvings: RIF pain when LIF palpated
Psoas sign: RIF pain on right hip extension
Palpable mass if abscess present
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40
Q

What are some signs, symptoms and blood results that would indicate the need for an appendicectomy?

A
migration of pain
N&V
Rebound tenderness
Fever
neutrophil predominate leukocytosis
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41
Q

Define a hernia

A

protrusion of viscera from its containing cavity

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42
Q

Describe the anatomy of a direct and indirect inguinal hernia

A

direct: enters through a defect in the posterior wall of the inguinal canal at Hesselbachs
indirect: enters through the deep ring and travels through the canal exiting at the superficial ring

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43
Q

How do you differentiate between a direct and indirect inguinal hernia?

A

Direct are found medial to IEVs

Indirect are found lateral to IEVs

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44
Q

How do you differentiate between an inguinal vs a femoral hernia?

A

inguinal are superior to the pubic tubercle
inguinal head towards the groin

femoral are infero-lateral to the pubic tubercle
femoral head straight down the leg
femoral are medial to the pulse

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45
Q

How would an obturator hernia present?

A

mass in the upper medial thigh

nerve compression = pain on hip extension, medial rotation and abduction

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46
Q

What are some differentials for hernias?

A

lymphadenopathy
aneurysm
saphena varix

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47
Q

How are hernias managed?

A

weight loss

open repair: generally if one off unilateral
laparoscopic repair: generally if recurrent, females, young, bilateral

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48
Q

What are some complications of hernias? Describe briefly what these terms mean

A

obstructed: bowel contents within the hernia becomes obstructed
incarcerated: contents is stuck inside the sack because of adhesions. The hernia can’t be reduced
strangulated: ischaemia of the tissue within the hernia

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49
Q

How would a strangulated hernia present?

What should you not do whilst awaiting surgery?

A

Pain out of proportion
Fever
Erythema of the overlying skin
Peritonitic features: guarding

Do not try to reduce it - this can lead to generalised peritonitis

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50
Q

Describe the types of hiatus hernias

A

sliding: gastroduodenal junction moves above the diaphragm in to the thoracic cavity
rolling: gastroduodenal junction remains in the abdomen but the fundus herniates in to the thoracic cavity

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51
Q

How does a hiatus hernia present?

What examination finding might you find?

A
reflux
dysphagia 
weight loss 
hiccups 
vomiting
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52
Q

How are hiatus hernias managed?

A

weight loss, stop smoking, stop alcohol
PPIs
fundoplication

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53
Q

What would you see at endoscopy of a hiatus hernia?

A

upward displacement of the z-line

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54
Q

What are some complications of fundoplication for hiatus hernia?

A

recurrence of the hernia
dysphagia if done too tightly
bloating - inability to belch
fundal necrosis

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55
Q

What is a complication of a rolling hiatus hernia? How would this present?

A

gastric volvulus

  • Inability to pass an NG tube
  • Retching but no vomiting
  • Pain
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56
Q

What is diverticulosis, diverticular disease and diverticulitis?

A

diverticulosis: outpouchings of mucosa between the teniae coli
disease: symptoms arising from the diverticulosis
diverticulitis: inflammation and infection of the diverticulosis often due to faces and food getting stuck in the neck of the outpouching

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57
Q

Where does diverticulosis most commonly occur?

A

sigmoid colon

can also be descending colon

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58
Q

What are the causes/risk factors for developing diverticulosis?

A

low fibre diet and constipation

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59
Q

What are the symptoms of diverticular disease?

A

erratic bowel habits: constipation and diarrhoea
painless bleeding
Colicky LIF pain that is relieved by defecation

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60
Q

How is diverticular disease managed?

How and when is acute diverticulitis managed?

A

increased fibre
laxatives
analgesia

If >72 hours with no improvement or if severe
- NBM, IV fluids, IV metronidazole + a cephalosporin

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61
Q

How does acute diverticulitis present?

A
LIF pain
N&V
Erratic bowel habits  
Fever
Painful bleeding 
Abdominal distension
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62
Q

What are some complications of diverticular disease?

A
Fistula 
- vaginal = brown discharge
- bladder = frothy urine and UTIs
Perforation 
Strictures 
Haemorrhage (erosion in to vessels)
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63
Q

Compare the 2 histological subtypes of oesophageal cancer, their locations and the risk factors for them

A

squamous cell: upper 2/3rds
- alcohol, smoking, achalasia, reduced vit A

adeno: lower 1/3rd
- obesity, fatty diet, GORD

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64
Q

What are the red flags 2 week wait criteria for oesophageal cancer?

A

Dysphagia!! +

>55 with dyspepsia and weight loss

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65
Q

Compare Mallory Weiss and Boerhave

A

Mallory Weiss: superficial mucosa tear

Boerhave: full thickness oesophageal tear

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66
Q

How would an oesophageal tear present?

A

Retrosternal pain
Respiratory distress
Subcutaneous emphysema

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67
Q

How is oesophageal tear investigated? What would you see?

A

CT CAP with IV and oral contrast

- can see the oral contrast leaking out

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68
Q

How is oesophageal tear managed?

A

repair the tear
decontaminate the mediastinum and pleural cavity
abx
feeding via jejunostomy

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69
Q

What is achalasia?

A

failure of the LOS to relax
eventual failure of the oesophageal smooth muscle
this leads to the food bolus getting stuck
proximal damage of the oesophagus due to force against a blockage

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70
Q

How does achalasia present?

A

dysphagia to solids and liquids
weight loss
regurgitation
chest pain

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71
Q

How would you investigate achalasia? What would the results be?

A

Barium swallow
- bird beak appearance, dilated oesophagus, fluid level

CXR
- widened mediastinum

Oesophageal manometry
- failure of peristalsis, high LOS resting pressure and failure of it to relax

72
Q

How is achalasia managed?

A
Pneumatic balloon dilation 
Surgical - Hellers cardiomyotomy 
Botox into the LOS
CCBs and nitrates (little effect)
Small meals and sleep with ++pillows
73
Q

What is diffuse oesophageal spasm?

A

multifocal, high amplitude spasms due to dysfunctional oesophageal inhibitory nerves

74
Q

How would you investigate diffuse oesophageal spasm? What would the results be?

A

barium swallow
- see a corkscrew oesophagus
oesophageal manometry
- repetitive, simultaneous, ineffective contractions

75
Q

How is diffuse oesophageal spasm managed?

A

CCBs and nitrates

76
Q

What dose plummer-vinson consist of?

A

Dyspahgia due to oesophageal webs
Glossitis
Iron deficiency anaemia

77
Q

How is plummer-vinson managed?

A

dilation of the webs

iron

78
Q

A diabetic patient presents with an IBS picture, what could it be?
Who else is at risk of this condition?

A

Small bowel bacterial overgrowth

Scleroderma patients

79
Q

How is small bowel bacterial overgrowth managed?

A

Rifaxamin

80
Q

Where are most gastroenteropancreatic neuroendoctine tumours found?

A

small intestine

sometimes stomach and rectum

81
Q

In whom and how do gastroenteropancreatic neuroendoctine tumours present?

A

MEN 1, neurofibromatosis 1, tuberous sclerosis

non specific abdominal signs and symptoms

82
Q

What is carcinoid syndrome?

A

over due to liver metastasis there is secretion of serotonin +/- prostaglandins, gastrin and ACTH

83
Q

How does carcinoid syndrome present?

A

Flushing
Diarrhoea
Wheeze
Palpitations, tricuspid insufficiency, pulmonary stenosis

84
Q

How do you investigate carcinoid syndrome?

A

urine 5-HIAA

plasma chromogranin A

85
Q

How does a carcinoid crisis present?

A

Extremely low BP

86
Q

How is carcinoid syndrome managed?

A

octreotide - somatostatin analogue

87
Q

What is a pseudo-obstruction?

A

dilation of the bowel with no obstructive cause

88
Q

What can cause pseudo-obstruction?

A
Hypercalcaemia and hypomagnesemia
opioids and CCBs
post-surgical 
hypothyroidism 
Neurological: MS and Parkinsons
89
Q

How is a pseudo-obstruction managed?

A

endoscopic decompression

neostigmine

90
Q

How does volvulus present? Symptoms and key examination finding

What in the history would point towards a caecal volvulus rather than the classic sigmoid?

A

Abdominal distension
absolute constipation
Colicky pain

Tympanic on percussion

caecal: adhesions so previous surgery or pregnancy

91
Q

What is a volvulus?

A

Twisting of the intestine on its mesentery leading to obstruction and a reduced blood supply so necrosis

92
Q

How is volvulus managed?

A

decompress with a flatus tube

may need resection with Hartman’s if necrotic bowel or perforation

93
Q

What can cause acute mesenteric ischaemia? Therefore what are the risk factors?

A
  • Atherosclerosis
  • Embolism: AF, AAA, prosthetic valve, post-MI, hypercoagulable (including malignancy)
  • Non-occlusive: shock
94
Q

How does acute mesenteric ischaemia present?

A

Pain out of proportion
N&V
Bloody diarrhoea

95
Q

What ABG results would indicate acute mesenteric ischaemia?

A

raised lactate

acidotic

96
Q

How is acute mesenteric ischaemia imaged? What would you see?

A

Contrast CT

  • bowel wall oedema
  • gas within the bowel wall
  • reduced bowel wall enhancement
97
Q

How is acute mesenteric ischaemia managed?

A

Abx in case of perforation
Bowel excision if necrotic
Mesenteric angioplasty

98
Q

What is the cause of chronic mesenteric ischaemia?

A

atherosclerosis

99
Q

What in the history would suggest chronic mesenteric ischaemia?

A

cardiovascular risk factors
post-prandial pain
weight loss due to the pain and malabsorption

100
Q

How is chronic mesenteric ischaemia diagnosed and managed?

A

CT angiogram

Mesenteric angioplasty and stent

101
Q

What stain and shape is C-Diff?

A

Gram +ve

Rod

102
Q

What commonly causes c-diff infection?

A

Cephalosporins (ceftriaxone or clindamycin)

PPIs increase a patients risk

103
Q

What can c-diff infection lead to?

A

pseudomembranous colitis

104
Q

How would you investigate ?c-diff and what would the results be?

A

Bloods: ++WCC
C-Diff antigen: shows exposure not necessarily acute infection
C.diff toxin in stool

AXR: thumbprinting + loss of bowel wall architecture

105
Q

How is c-diff managed?

A
  1. Metronidazole

2. recurrent or severe: Vancomycin

106
Q

What is melanosis coli? What causes it?

A

pigmentation of the bowel wall

due to laxative abuse

107
Q

Disease of the rectum requires what surgery and/or anastomoses or stoma?

A

Anterior resection

Can do colorectal anastomoses or a defunctioning stoma

108
Q

When is an abdo-perineal resection required?

A

Involvement of the anal verge
Involvement of the sphincter
Disease within 2cm of the dentate line

109
Q

What are haemorrhoids? Where on PR examination would you classically see them?

A

Enlarged vascular cushions

At 3, 7 and 11 o’clock

110
Q

What are the grades of haemorrhoids?

A

1: don’t prolapse
2: prolapse on defecation but spontaneously reduce
3: manually reduce
4: don’t reduce

111
Q

Internal haemorrhoids are defined as what?

A

Originating above the dentate line

112
Q

What management options are available for haemorrhoids?

A

Increased fibre diet
Laxatives
Local anaesthetic creams

Rubber band ligation
Haemorrhoid artery ligation
Haemorrhoidectomy

113
Q

How do haemorrhoids present?

A

Pruritis
Painless rectal bleeding not mixed in with stool
Feeling of rectal fullness

114
Q

Haemorrhoids can thrombose, how would this present?

A

++ pain and tenderness

Oedematous, purple lump on examination

115
Q

What is a pilonidal sinus?

A

a sinus within the buttock cleft region that starts with an inflamed hair follicle

116
Q

In whom and how would a pilonidal sinus present?

A

Sweaty, hairy, sit down a lot, obese, poor hygiene

Often cyclical:
Red, painful swelling in the buttock cleft region
Discharge

117
Q

How is a pilonidal sinus managed?

A

Drain any abscess
Abx
Shave

118
Q

What is a perianal fistula and what are the causes/risk factors?

A

Connection between the anus and the skin of the perineum

Recurrent abscesses
IBD
TB and HIV
radiation to the area

119
Q

How does a perianal fistula present?

A

Recurrent abscesses

Discharge on to the skin

120
Q

How are perianal fistulas managed?

A

Fistulotomy

Seton

121
Q

What are the types of anorectal abscesses?

A

perianal
intersphinteric
ischiorectal
supralevator

122
Q

How do anorectal abscess present?

A

Pain on sitting down
Swelling or hard lump felt
Discharge
+/- Cellulitis and systemically unwell

123
Q

How are anorectal abscesses managed?

A

Incision and draining

Antibiotics

124
Q

What is an anal fissure?

A

Tear in the mucosal lining of the anal canal

125
Q

What are the risk factors for anal fissures?

A

Constipation (and therefore dehydration)

IBD

126
Q

How do anal fissures present?

A

Pain on defecation that can last for hours
Fresh rectal blood
Itch

127
Q

How are anal fissures managed?

A

Increase fluid and fibre intake
Bulk forming laxatives
Lubricants
Topical local anaesthetics

> 6 weeks of symptoms = GTN cream

8 weeks of GTN = sphincterotomy

128
Q

AV malformations in the large bowel are known as what? How do they present?

A

Angiodysplasia

Painless PR bleed

129
Q

Describe a partial vs a full rectal prolapse

A

partial: rectal mucosa prolapses out of the anus
full: rectal wall prolapses out of the anus

130
Q

What are the risk factors for rectal prolapses?

A

Constipation
Long standing haemorrhoids
Childbirth
Cough

131
Q

How do rectal prolapses present?

A

Initially a feeling of fullness and tenesmus

Faecal incontinence
Discharge
Bleeding and ulceration

132
Q

How are rectal prolapses managed?

A

Increased fluid and fibre

Surgical management

133
Q

What are the histological subtypes of anal cancer?

A

above dentate: adenocarcinoma

below dentate: squamous cell carcinoma

134
Q

What are the risk factors for anal cancer?

A

HPV 16 and 18
HIV
IBD
immunosuppressed

135
Q

How does rectal cancer present?

A
Painful rectum
Bleeding
Palpable mass
Itch
Discharge
136
Q

Which lymph nodes does anal cancer spread to?

A

Proximal: pelvic

Anal margin: inguinal

137
Q

Where does the spleen get its blood supply from?

A

splenic and left gastroepiploic

138
Q

What are the causes of a splenic infarct?

A

Embolism: AF and post-MI

Abnormal blood: Sickle cell, CML, myelofibrosis

139
Q

How would a splenic infarct present?

A

LUQ pain

+/- fever, N&V

140
Q

How would you investigate a ?splenic infarct and what would this show?

A

CT with contrast

Hypo-attenuated wedge shaped area

141
Q

How is a splenic infarct managed in the short and long term?

A

Immediate: treat the underlying cause

Long term: long term penicillin + pneumonia, influenza and meningitidis vaccines

142
Q

What are the causes of splenic rupture?

A

Trauma

Massive splenomegaly

143
Q

How does a splenic rupture present?

A

Shock
Peritonism
LUQ and shoulder tip pain

144
Q

Someone comes in with a ruptured spleen and is unstable, what do you do?

A

Immediate laparotomy

145
Q

Someone comes in with a ruptured spleen and is stable, what do you do?

A

CT CAP
Permissive hypotension
Vessel embolization

146
Q

What are the complications of a splenic rupture and its management?

A

Necrosis
Abscess
DVT and PE (thrombocytosis)
Overwhelming post-splenectomy infection

147
Q

What is the macroscopic and microscopic appearance of Crohns disease?

Where does it most commonly affect?

A

Macro: skip lesions, cobblestone (deep ulcers and fissures)
Micro: non-caseating granulomas, increased goblet cells

Location:
From mouth to anus
It most commonly affects the terminal ileum and proximal colon

148
Q

How would Crohns disease present?

A
Abdominal pain
!Weight loss! 
mucous diarrhoea (+/- blood)
Malaise (B12 and iron deficiency)
Oral ulcers
Perianal fistula
Skin tags
149
Q

What are the dermatological manifestations of Crohns disease?

A

Pyoderma gangrenosum
- ulcers on the legs
Erythema nodosum
- tender, subcutaneous nodules on the shins

150
Q

Aside from dermatological, what are the other extra-colonic manifestations of Crohns disease?

A

Episcleritis
Sacroiliac arthritis (arthritis is most common manifestation)
Renal stones (oxalate)
!Gallstones!

151
Q

What bloods results would you expect in IBD?

A

B12 deficient
Raised CRP and WCC
Hypalbuminaemia (poor absorption)

152
Q

Aside from bloods and imaging how else is IBD diagnosed?

A

Faecal calprotectin

153
Q

Which type of endoscopy is first line in ?Crohns vs ?UC

A

Crohns: colonoscopy
UC: flexible sigmoidoscopy

154
Q

How is remission of Crohns induced?

A

Stop smoking!

  1. Steroids
    2: Mesalazine
    3: + Azathiorprine or methotrexate or mercaptopurine
    4: infliximab
155
Q

Once in remission, what is the management of Crohns

A

1: Azathioprine or mercaptopurine
2: Methotrexate

156
Q

Aside from immunosuppressing drugs, what else must you remember to give in an IBD flare?

A

Heparin as they are pro-thrombotic

157
Q

Where does UC affect? Location and layers

A

Begins in the rectum and spreads proximally
Never spreads beyond ileocecal valve

Mucosa and submucosa only

158
Q

What is the macro and microscopic appearance of UC?

A

Macro: crypt abscesses and pseudopolyps (inflamed tissue due to cycle of ulcers and healing)

Micro: decreased goblet cells

159
Q

How does UC present?

A

Abdominal pain
Bloody diarrhoea +/- mucous
Tenesmus
Malaise

160
Q

How would you categorise the severity of UC?

A

Truelove and Wit

mild: <4 stools/day
moderate: 4-6 stools/day +blood
severe: >6 stools/day + blood + systemic upset (fever, tachycardia, anaemia)

161
Q

How is a mild or moderate flare of UC managed?

A

Just left sided disease

  1. topical aminosalicylates
  2. add oral after 4 weeks
  3. topical or oral steroids

Extensive disease

  • Topical AND oral aminosalicylates (mesalazine)
  • Add oral steroids
162
Q

How is a severe flare of UC managed?

A

IV steroids
+ IV ciclosporin if no improvement after 72 hours
+ infliximab

163
Q

Once in remission, how is UC managed?

A

Topical or oral aminosalicylates (mesalazine)

164
Q

If a patient suffers >2 flares of UC per year, what management is considered?

A

oral azathioprine or mercaptopurine

165
Q

How would toxic megacolon present?

A

Fever + distension + pain

166
Q

What are the extra colonic manifestations of UC?

A

Arthritis
Primary sclerosing cholangitis
Anterior uveitis
Erythema nodosum

167
Q

Compare the appearance of Crohns and UC on barium enema

A

Crohns:

  • long strictured segment seen as “Kantors string sign”
  • ulcers
  • proximal bowel dilation
  • fistulae

UC:

  • loss of haustra
  • “lead pipe” thin and no short
  • superficial ulceration seen as pseudopolyps
168
Q

What are the complications of Crohns and its management?

A
Fistulae
Abscesses
Strictures leading to obstruction
Small bowel and colorectal cancer
Osteoporosis 
Short bowel syndrome as a result of multiple small bowel resections
169
Q

What are the symptoms of GORD?

A

dyspepsia - burning
acid taste in the mouth
regurgitation
cough

170
Q

How is GORD managed?

A

Full dose PPI for 1 month

Then lower tailored dose

171
Q

If a GORD patient is going for endoscopy what do you need to tell them about their medication?

A

Stop their PPI 2 weeks before

172
Q

What are the complications of GORD?

A

Pneumonia
Cancer
Barret’s oesophagus

173
Q

What is Barret’s oesophagus?

A

Metaplasia of stratified squamous epithelium to glandular simple columnar

174
Q

Describe the OGD findings in Barret’s oesophagus

A

Red and velvety appearance

175
Q

Before an appendicectomy what needs to be done for the patient?

A

Prophylactic IV abx to reduce wound infection rates