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Surgery > General > Flashcards

General Flashcards

1
Q

Explain acute abdomen due to perforated viscus

A

Get peritonitis

Causes of perforation: peptic ulcer, small/large bowel obstruction, diverticular disease, inflammatory bowel disease

Presentation: lying completely still, looking unwell

Examination: tachycardia, hypotension, completely rigid abdomen, involuntary guarding, reduced/absent bowel sounds

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2
Q

Give an overview of ischaemic bowel

A

Severe pain, out of proportion to clinical signs (ischaemic bowel until proven otherwise)

Acidaemia, raised lactate

Diffuse, constant pain

Need CT with contrast for diagnosis

Need early surgical involvement

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3
Q

What are the differentials for RUQ pain

A

Cholecystitis

Pyelonephritis

Ureteric colic

Hepatitis

Pneumonia

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4
Q

What are the differentials for LUQ pain

A

Gastric ulcer

Pyelonephritis

Ureteric colic

Pneumonia

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5
Q

What are the differentials for RLQ pain

A

Appendicitis

Ureteric colic

Inguinal hernia

IBD

UTI

Gynaecological

Testicular torsion

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6
Q

What are the differentials for LLQ pain

A

Diverticulitis

Ureteric colic

Inguinal hernia

IBD

UTI

Gynaecological

Testicular torsion

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7
Q

What are the differentials for epigastic pain

A

Peptic ulcer disease

Cholecystitis

Pancreatitis

MI

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8
Q

What are the differentials for peri-umbilical pain

A

Small bowel obstruction

Large bowel obstruction

Appendicitis

Abdominal aortic aneurysm

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9
Q

What investigations are needed for acute abdomen

A

Urine dip

Pregnancy test

ABG

Bloods (+ amylase for pancreatitis)

Blood cultures

Erect CXR

Ultrasound (KUG, biliary tree, gynae)

CT

ECG (rule out referred cardiac pain)

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10
Q

What initial management is needed for acute abdomen

A

Get IV access

Nil by mouth

Analgesia

Antiemetics

VTE prophylaxis

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11
Q

What are the emergency causes of haematemesis

A

Oesophageal varices

Gastric ulceration

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12
Q

Give an overview of oesophageal varices as a cause of haematemesis

A

Dilated porto-systemic venous anastomoses in oesophagus

Dilated veins are: swollen, thin-walled, prone to rupture

Can cause catastrophic haemorrhage

Common underlying cause (portal hypertension - alcoholic liver disease)

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13
Q

Give an overview of gastric ulceration as a cause of haematemesis

A

60% haematemesis cases

Erosion of blood vessels in lesser curve of stomach/posterior duodenum

May present with: known active ulcer disease, H pylori positive, NSAID use, steroid use, previous symptoms of peptic ulcer

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14
Q

What are the non-emergency causes of haematemesis

A

Mallory-Weiss tears

Oesophagitis (inflammation of intraluminal epithelial layer, mostly due to GORD)

Gastritis

Gastric malignancy

Meckel’s diverticulum

Vascular malformation

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15
Q

What scoring systems are used in haematemesis

A

Glasgow-Blatchford bleeding score (based on clinical and biochemical features, >6 = 50% risk of needing intervention)

MIN 65 score (for in-hospital mortality from upper GI bleed)

Rockall score (for GI bleed post-endoscopy)

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16
Q

What investigations are needed for haematemesis

A

Routine blood (+clotting)

VBG

Group and save

Oesophago-gastro-duodenoscopy (within 12 hrs of acute haematemesis)

Erect CXR (if suspect perforated peptic ulcer)

CT with contrast

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17
Q

What is the management of haematemesis due to peptic ulcer disease

A

Injection of adrenaline

Cauterise bleed

Give high dose PPI

H pylori eradication (if needed)

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18
Q

What is the management of haematemesis due to oesophageal varices

A

Endoscopic banding

Start somatostatin analogue or vasopressin (reduce splanchnic blood flow)

Long term management: repeat banding, long term beta blocks

Severe bleeds: Sengstaken-Blakemore tube (insert at level of varices, inflate to compress vessel)

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19
Q

What are the mechanical causes of dysphagia

A

Oesophageal/gastric malignancy

Benign oesophageal strictures

Extrinsic compression

Pharyngeal pouch

Foreign body

Oesophageal web

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20
Q

What are the neuromuscular causes of dysphagia

A

Post-stroke

Achalasia

Diffuse oesophageal spasm

Myasthenia gravis

Myotonic dystrophy

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21
Q

What investigations are needed in dysphagia

A

Endoscopy

Routine bloods

Consider manometry and 24 hr pH studies

Consider 2ww

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22
Q

What are the 2ww guidelines for GI malignancy

A

Urgent upper GI endoscopy

For people with dysphagia or those who are > 55 and have weight loss and one of: upper abdo pain, reflux, dyspepsia

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23
Q

What is the management for dysphagia

A

Treat underlying cause

Malignancy: surgery, chemotherapy, palliation

Motility disorders: refer for swallowing therapy

If no immediate reversible cause found, refer to SALT and dieticians

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24
Q

What is bowel obstruction

A

Mechanical blockage of bowel

One bowel segment occluded, gross dilation of proximal parts, increased peristalsis, secretion of large volume of electrolyte-rich fluid into bowel (third spacing)

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25
Q

What is closed loop bowel obstruction

A

Obstruction in 2 places

Surgical emergency

Bowel wall stretches, get ischaemia or perforation

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26
Q

What are the causes of bowel obstruction

A

Small bowel: adhesions, hernia

Large bowel: malignancy, diverticular disease, volvulus

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27
Q

In what locations can bowel obstructions occur

A

Intramural (gallstone ileus, faecal impaction, foreign body)

Mural (cancer, strictures, intussusception, lymphoma)

Extramural (hernia, adhesions, volvulus)

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28
Q

How might bowel obstruction present

A

Colicky/cramping abdominal pain

Vomiting (early in proximal, late in distal)

Abdominal distension

Absolute constipation

Tinkering bowel sounds

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29
Q

What are the differentials for bowel obstruction

A

Pseudo-obstruction

Paralytic ileus

Toxic megacolon

Constipation

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30
Q

What investigations are needed for bowel obstruction

A

Urgent bloods

VBG (high lactate in ischaemia)

CT with contrast (preferred)

Abdominal X-ray

Erect CXR

Water-soluble contrast study

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31
Q

What are the signs of small bowel obstruction on X-ray

A

> 3 cm bowel

Central abdominal location

Valvulae conniventes visible (lines completely crossing bowel)

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32
Q

What are the signs of large bowel obstruction on X-ray

A

> 6 cm bowel

> 9 cm caecum

Peripheral location

Haustra lines visible

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33
Q

What is the management for bowel obstruction

A

Urgent fluid resuscitation

If ischaemia/closed loop, urgent surgery

‘Drip and suck’ (NBM, decompress bowel by sucking, start IV fluids)

Catheter

Analgesia

Antiemetics

Virgin abdomens usually need surgery

Surgery: ischaemia, closed loop, strangulated hernias, obstructing tumours, failure to improve in 48 hrs

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34
Q

What are the complications of bowel obstruction

A

Bowel ischaemia

Bowel perforation

Dehydration

Renal impairment

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35
Q

What are the causes of GI perforation

A

Peptic ulcer

Sigmoid diverticulum

Foreign body

Diverticulitis

Cholecystitis

Meckel’s diverticulum

Mesenteric ischaemia

Toxic megacolon

Trauma

Excessive vomiting

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36
Q

How might GI perforation present

A

Rapid onset sharp pain

Systemically unwell

Features of sepsis

Peritonitic

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37
Q

What are the differentials for GI perforation

A

Acute pancreatitis

Myocardial infarction

Tubo-ovarian pathology

Ruptured aortic aneurysm

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38
Q

What investigations are needed for GI perforation

A

Routine bloods

Urinalysis

Erect CXR

CT (gold standard)

Abdominal X-ray

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39
Q

What are the signs of GI perforation on abdominal X-ray

A

Rigler’s sign: both sides of bowel wall seen (intra-abdominal air acts as additional contrast)

Psoas sign: loss of sharp delineation of psoas muscle border (fluid in retroperitoneal space)

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40
Q

What is the management for GI perforation

A

Resuscitation

Start broad spectrum antibiotics early

NBM

Most will need surgery

Some may just need conservative management

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41
Q

What are the complications of GI perforation

A

Infection

Haemorrhage

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42
Q

What are the causes of melena

A

Peptic ulcer disease

Variceal bleed

Upper GI malignancy

Gastritis

Oesophagitis

Mallory-Weiss tears

Meckel’s diverticulum

Vascular malformations

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43
Q

What investigations are needed for melena

A

Routine bloods (+ clotting + group and save)

ABG

Oesophago-gastro-duodenoscopy

CT abdo with contrast

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44
Q

What is the management for melena

A

A to E

Arrange endoscopy

If haemodynamically unstable: transfuse, correct deranged coagulation

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45
Q

Which scoring system is used for lower GI bleeds

A

Oakland score

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46
Q

What are the risk factors for adverse outcomes for rectal bleeding

A

Haemodynamic instability

Ongoing haematochezia

> 60

Serum creatinine > 150

Significant comorbidities

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47
Q

What are the differentials for rectal bleeding

A

Diverticular disease

Ischaemic colitis

Infective colitis

Haemorrhoids

Malignancy

Angiodysplasia

Crohn’s disease

Ulcerative colitis

Radiation proctitis

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48
Q

What investigations are needed for rectal bleeding

A

Routine bloods (+ clotting + group and save)

Stool culture

If unstable, stabilise then CT angiogram (localise bleed)

Fixed sigmoidoscopy/colonoscopy

OGD/MRI

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49
Q

What is the management for rectal bleeding

A

95% settle spontaneously

A to E

If Hb < 70, transfuse packed RBCs

Reverse anticoagulants

Endoscopic haemostasis: inject adrenaline, banding

Arterial embolisation

Surgery rarely needed

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50
Q

What is the pathophysiology of GORD

A

High frequency of sphincter relaxations of lower oesophageal sphincter

Get reflux of gastric contents into oesophagus

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51
Q

What are the risk factors for GORD

A

Age

Obesity

Male

Alcohol

Smoking

Caffeinated drinks

Fatty/spicy food

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52
Q

How might GORD present

A

Burning retrosternal pain

Worse on lying/bending/eating

Excessive belching

Odynophagia

Chronic cough

Nocturnal cough

Red flags: dysphagia, weight loss, early satiety, malaise, loss of appetite

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53
Q

What classification system is used for GORD

A

Los Angeles classification

Grades reflux oesophagitis

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54
Q

What are the differentials for GORD

A

Malignancy

Peptic ulcer

Oesophageal motility disorders

Oesophagitis

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55
Q

What investigations are needed for GORD

A

Usually clinical diagnosis

24 hr pH monitoring

Upper GO endoscopy

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56
Q

What is the management for GORD

A

Initial: avoid precipitants, weight loss, smoking cessation

PPIs

Surgery (in failure of PPIs/complications): fundoplication

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57
Q

What are the complications of GORD

A

Aspiration pneumonia

Barret’s oesophagus

Oesophagitis

Oesophageal strictures

Oesophageal cancer

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58
Q

What is Barrett’s oesophagus

A

Metaplasia of oesophageal epithelial lining

Stratified squamous –> simple columnar

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59
Q

What are the risk factors for Barrett’s oesophagus

A

Caucasian

Male

> 50

Smoking

Obesity

Hiatus hernia

Family history

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60
Q

How might Barrett’s oesophagus present

A

History of GORD

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61
Q

What investigations are needed for Barrett’s oesophagus

A

Take biopsy during OGD (red, velvety)

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62
Q

What is the management for Barrett’s oesophagus

A

Start PPI

Stop medications that impact stomach’s protective barrier (NSAIDs…)

Lifestyle advice

Regular endoscopies (3 months - 5 years) to monitor for progression to adenocarcinoma

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63
Q

What are the 2 types of oesophageal cancer

A

Squamous cell carcinoma

Adenocarcinoma

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64
Q

How might oesophageal cancer present

A

Dysphagia

Weight loss

Odynophagia

Hoarseness of voice

Cachexia

Dehydration

Supraclavicular lymphadenopathy

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65
Q

What investigations are needed for oesophageal cancer

A

Urgent OGD

Staging CT

Endoscopic ultrasound

Staging laparoscopy

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66
Q

What is the prognosis for oesophageal cancer

A

5 year survival 5-10%

Palliative patients have median survival of 4 months

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67
Q

How might oesophageal tears present

A

Severe, sudden-onset retrosternal pain

Respiratory distress

Subcutaneous emphysema

Following severe vomiting/retching

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68
Q

What investigations are needed for oesophageal tears

A

Routine bloods (+ clotting + group and save)

CXR

CT chest and abdo

Endoscopy

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69
Q

What is the management for oesophageal tears

A

Resuscitate

Control lead

Eradicate mediastinal/pleural contamination

Decompress oesophagus

Nutritional support

Surgery

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70
Q

What is achalasia

A

Failure of lower oesophageal sphincter to relax

Progressive failure of oesophageal smooth muscle to contract

Progressive destruction of ganglionic cells in myenteric plexus

Can get dysfunction of proximal oesophagus

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71
Q

How might achalasia present

A

Progressive dysphagia

Vomiting

Chest discomfort

Regurgitation

Coughing

Weight loss

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72
Q

What investigations are needed for achalasia

A

MRI (bird beak image)

OGD (exclude oesophageal cancer)

Oesophageal manometry (measures pressure in oesophageal sphincter)

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73
Q

What is the management of achalasia

A

Sleep with many pillows

Eat slowly

CCBs

Botox injections (into lower oesophageal sphincter)

Endoscopic balloon dilation

Laparoscopic Heller myotomy (division of fibres of the sphincter that is not relaxing)

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74
Q

Give an overview of diffuse oesophageal spasms

A

Multi-focal high amplitude contractions of oesophagus

Presentation: severe dysphagia, chest pain

Investigations: oesophageal manometry, barium swallow (corkscrew appearance)

Management: CCBs/nitrates (relaxation of oesophageal smooth muscle), pneumatic dilation, myotomy

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75
Q

What is a hiatus hernia

A

Protrusion of an organ from abdominal cavity into thorax through oesophageal hiatus

Stomach usually herniates

76
Q

What are the 2 types of hiatus hernia

A

Sliding (organ slides up through diaphragmatic hiatus)

Rolling (creates a ‘bubble’ of stomach in thorax)

77
Q

What are the risk factors for hiatus hernia

A

Age

Pregnancy

Obesity

Ascites

78
Q

How might hiatus hernia present

A

Most asymptomatic

GORD

Vomiting

Weight loss

Bleeding

Hiccups

Palpitations

Dysphagia

Might hear bowel sounds in chest (if hernia very large)

79
Q

What are the differentials for hiatus hernia

A

Cardiac chest pain

Malignancy (gastric, pancreatic)

GORD

80
Q

What are the investigations for hiatus hernia

A

OGD (gold standard, see upward displacement of gastro-oesophageal junction)

Incidental finding on CT/MRI

81
Q

What is the management for hiatus hernia

A

PPIs

Lifestyle modification (weight loss, sleep with head raised)

Cruroplasty (hernia reduced from thorax into abdomen, may need mesh)

Fundoplication (fundus wrapped around lower oesophageal sphincter)

82
Q

What are the complications of hiatus hernia

A

Incarceration/strangulation

Gastric volvulus (stomach twists on itself, get necrosis)

Complications of surgery: recurrence, bloating, dysphagia (fundoplication too tight), fundal necrosis

83
Q

What is Borchardt’s triad

A

Seen in gastric volvulus

Severe epigastric pain

Retching without vomiting

Inability to pass NG tube

84
Q

What is peptic ulcer disease commonly related to

A

H pylori infection

NSAID use

85
Q

What are the risk factors for peptic ulcer disease

A

H pylori infection

Prolonged NSAID use

Corticosteroid use

Previous gastric bypass

Physiological stress

Head trauma

Zollinger-Ellison syndrome (severe peptic ulcer disease, gastric acid hypersecretion, gastrinoma)

86
Q

How might peptic ulcer disease present

A

Epigastric pain

Retrosternal pain

Nausea

Bloating

Post-prandial discomfort

Early satiety

Complications of ulcer: bleeding, perforation, gastric outlet obstruction

87
Q

What are the differentials for peptic ulcer disease

A

Acute coronary syndrome

GORD

Gallstones

Gastric malignancy

Pancreatitis

88
Q

What investigations are needed for peptic ulcer disease

A

Routine bloods

H pylori testing (urea breath test, serum antibodies, stool antiges)

OGD

Biopsy

89
Q

What are the NICE guidelines for investigating peptic ulcer disease

A

All identified ulcers should be biopsied (malignant potential)

Repeat endoscopy towards end of PPI therapy (check for resolution)

90
Q

What is the management for peptic ulcer disease

A

Lifestyle advice

PPI

Have H pylori: PPI + amoxicillin + clarithromycin/metronidazone

Surgery rarely needed (only in perforations or very severe disease)

91
Q

What are the complications of peptic ulcer disease

A

Perforation

Haemorrhage

Pyloric stenosis

92
Q

What are the risk factors for gastric cancer

A

Male

H pylori infection

Increasing age

Smoking

Alcohol

Salty diet

Family history

Pernicious anaemia

93
Q

How might gastric cancer present

A

Dyspepsia

Dysphagia

Early satiety

Vomiting

Melena

Anorexia

Weight loss

Anaemia

Epigastric mass

Virchow’s node

Hepatomegaly

Ascites

Jaundice

94
Q

What are the differentials for gastric cancer

A

Peptic ulcer disease

GORD

Gallstones

Pancreatic cancer

95
Q

What investigations are needed for gastric cancer

A

Bloods

OGD

Staging CT

96
Q

What are the 2 types of inguinal hernia

A

Direct: bowel goes directly into inguinal canal, through weakness in Hesselbach’s triangle, more in older people, medial to inferior epigastric vessel

Indirect: bowel enters inguinal canal through deep inguinal ring, due to incomplete closure of processus vaginalis, lateral to inferior epigastric vessel

97
Q

What are the risk factors for inguinal hernia

A

Male

Increasing age

Raised intra-abdominal pressure: chronic cough, heavy lifting, chronic constipation

Obesity

98
Q

How might inguinal hernia present

A

Lump in groin

In incarcerated: painful, tender, erythematous

If strangulated: blood supply compromised, irreducible, tender, pain out of proportion to clinical signs

Features of bowel obstruction

99
Q

How do you differentiate between direct and indirect inguinal hernias

A

Reduce hernia

Press over inguinal ring

Ask patient to cough

If protrudes, direct

If doesn’t protrude, indirect

Only definitive way is to look during surgery

100
Q

What are the differentials for inguinal hernia

A

Femoral hernia

Saphena varix

Inguinal lymphadenopathy

Lipoma

Groin abscess

Internal iliac aneurysm

If extends into scrotum: hydrocele, varicocele, testicular mass

101
Q

What is the management for inguinal hernia

A

Indications: irreducible, incarcerated, obstructed, strangulated

Open/laparoscopic repair

102
Q

What are the complications of inguinal hernias

A

Incarceration

Strangulation

Obstruction

Post-op: pain, bruising, haematoma, infection, urinary retention, recurrence, chronic pain, damage to vas deferens/testicular vessels

103
Q

What are the risk factors for femoral hernia

A

Female

Pregnancy

Raised intra-abdominal pressure

Increasing age

104
Q

How might femoral hernia present

A

Small lump in groin

Infero-lateral to pubic tubercle (medial to femoral pulse)

105
Q

What are the differentials for femoral hernia

A

Inguinal hernia

Femoral canal lipoma

Saphena varix

Femoral artery aneurysm

Athletic pubalgia (small tear in rectus sheath, impingement of abdominal wall muscles)

106
Q

What investigations are needed for femoral hernia

A

Clinical diagnosis

May need ultrasound/CT

107
Q

What is the management for femoral hernia

A

Usually need surgery within 2 weeks of presentation (high strangulation risk)

Can have low or high surgical approach (below/above inguinal ligament)

108
Q

What is an epigastric hernia

A

Hernia in upper midline

Through fibres of linea alba

Due to chronic raised intraabdominal pressure

Mostly middle ages men

Usually asymptomatic

Disappears on lying flat

109
Q

What is a paraumbilical hernia

A

Herniation through linea alba, around umbilical region (not through umbilicus)

Due to chronic raised intraabdominal pressure

Contain pre-peritoneal fat

Do not usually strangulate

110
Q

What is a spigelian hernia

A

In semilunar line, around level of arcuate line

Small tender mass on lower lateral edge of rectus abdominis

High risk of strangulation

111
Q

What is an obturator hernia

A

Hernia of pelvic floor

Through obturator foramen, into obturator canal

Usually in elderly women

Mass in upper medial thigh

Features of small bowel obstruction

Positive Howship-Romberg sign (compression of obturator nerve)

112
Q

What is Littre’s hernia

A

Herniation of Meckel’s diverticulum

Mostly in inguinal canal

113
Q

What is a lumbar hernia

A

Rare

Posterior mass

Associated with back pain

114
Q

What is a Richter’s hernia

A

At any site

Partial herniation of bowel (anti-mesenteric border strangulated)

Tender, irreducible mass

Symptoms of obstruction

Surgical emergency

115
Q

What is hospital-acquired gastroenteritis

A

Usually C diff

Following broad spectrum antibiotics (disrupt normal microbiota)

Large amounts of enterotoxin A and B produced

Present with severe bloody diarrhoea

Can get toxic megacolon

Investigations: stool culture, C diff toxin test

Management: IV fluid rehydration, oral metronidazole. Start vancomycin if severe disease/no improvement after 72 hrs

116
Q

What is angiodysplasia

A

Most common vascular abnormality in GI tract

Formation of arteriovenous malformations between previously healthy blood vessels (often due to reduced submucosal venous drainage of colon)

117
Q

How might angiodysplasia present

A

Asymptomatic (diagnosed during colonoscopy)

Painless occult PR bleeding

Acute haemorrhage

118
Q

What are the differentials for angiodysplasia

A

Oesophageal varices

GI malignancy

Diverticular disease

Coagulopathies

119
Q

What investigations are needed for angiodysplasia

A

Routine bloods (+ clotting + group and save)

Upper GI endoscopy/colonoscopy (exclude malignancy)

Mesenteric angiography (to confirm diagnosis)

120
Q

What is the management for angiodysplasia

A

Conservative

Endoscopic argon plasma coagulation

Laser photoablation

Sclerotherapy

Band ligation

Surgery: resection and anastomosis of affected bowel segment (in severe bleeds or repeat recurrence)

121
Q

What are the complications of angiodysplasia treatment

A

Re-bleeding

Bowel perforation

Haematoma formation

Arterial dissection

Thrombosis

Bowel ischaemia

122
Q

What are gastroenteropancreatic neuroendocrine tumours (GEP-NETs)

A

Neuroendocrine tumours from neuroendocrine cells in tubular GI tract and pancreas

Classified grade 1 - 3: based on mitotic count

Also classified as functioning or non-functioning, based on whether there is hormone hypersecretion

123
Q

What are the risk factors for gastroenteropancreatic neuroendocrine tumours (GEP-NETs)

A

Multiple endocrine neoplasia type 1

Von Hipple-Lindau disease

Neurofibromatosis

Tuberous sclerosis

124
Q

How might gastroenteropancreatic neuroendocrine tumours (GEP-NETs) presents

A

Vague abdominal pain

Nausea and vomiting

Abdominal distension

Features of bowel obstruction

Weight loss

Palpable abdominal mass

125
Q

What investigations are needed for gastroenteropancreatic neuroendocrine tumours (GEP-NETs)

A

Chromogranin A and 5-HIAA levels

Routine bloods

Pancreatic peptides

Genetic testing

Endoscopy

126
Q

What is carcinoid crisis

A

Overwhelming release of hormones from gastroenteropancreatic neuroendocrine tumours (GEP-NETs)

Get resistant severe hypotension

Treat with somatostatin analogues

127
Q

What are the risk factors for acute appendicitis

A

Family history

Caucasian

Summer time

128
Q

How might acute appendicitis present

A

Acute abdominal pain (initially dull poorly localised, then sharp right iliac fossa)

Nausea and vomiting

Anorexia

Diarrhoea/constipation

Tachycardia, tachypnoea, pyrexia

Rebound tenderness over McBurney’s point (2/3 distance between umbilicus and asis)

Rovsing’s sign

Psoas sign

129
Q

What is Rovsing’s sign

A

Due to acute appendicitis

Right iliac fossa pain on palpation of left iliac fossa

130
Q

What is psoas sign

A

Due to acute appendicitis

Right iliac fossa pain extending to right hip

131
Q

What investigations are needed for acute appendicitis

A

Urinalysis

Routine bloods

Ultrasound

CT

132
Q

What is the management for acute appendicitis

A

Laparoscopic appendicectomy: definitive

If simple: antibiotics alone (high failure rates)

133
Q

What are the complications of acute appendicitis

A

Perforation

Surgical site infection

Appendix mass (omentum and small bowel adhere to appendix)

Pelvic abscess

134
Q

What is diverticular disease

A

Outpouching of bowel wall

Usually in sigmoid colon

Diverticulosis - presence of diverticula

Diverticular disease - symptoms from diverticula

Diverticulitis - inflammation of diverticula

Diverticula bleeding - diverticulum erodes into vessels (large volume, painless bleeding)

135
Q

What is the pathophysiology of diverticular disease

A

Weakened bowel

Movement of stool causes increased luminal pressure

Outpouching of mucosa through weakened area

Bacteria can grow in outpouchings

Diverticulum can perforate

136
Q

What are the differentials for diverticular disease

A

Age

Low fibre diet

Obesity

Smoking

Family history

NSAID use

M>F

137
Q

How might diverticular disease present

A

Intermittent colicky lower abdominal pain

Altered bowel habits

Nausea

Flatulence

138
Q

How might acute diverticulitis present

A

Acute sharp abdominal pain

Localised to left iliac fossa

Worse on movement

Systemic features

139
Q

How might perforated diverticulum present

A

Localised peritonitis

Generalised peritonitis

Extremely unwell

140
Q

What are the differentials for diverticular disease

A

Inflammatory bowel disease

Bowel cancer

Mesenteric ischaemia

Gynae causes

Renal stones

141
Q

What investigations are needed for diverticular disease

A

CT abdo-pelvis

Flexible sigmoidoscopy

142
Q

What are the CT findings in diverticular disease

A

Thickening of colonic wall

Pericolonic fat stranding

Abscess

Localised air bubble

Free air

143
Q

What classification system is used for diverticular disease

A

Hinchey classification

144
Q

How is diverticular disease managed

A

Analgesia, fluids, self-limiting bleeding

Acute diverticulitis: antibiotics, IV fluids, analgesia

Surgery: for perforation/faecal peritonitis/overwhelming sepsis, use Hartmann’s procedure

145
Q

What are the complications of diverticular disease

A

Recurrent diverticulitis

Diverticular stricture

Fistula formation

146
Q

What is pseudo-obstruction

A

Oglivie syndrome

Dilation of colon due to adynamic bowel, in absence of mechanical obstruction

Common in caecum and ascending colon

147
Q

What are the causes of pseudo-obstruction

A

Electrolyte imbalance

Endocrine disorder

Medications (opioids, CCBs, antidepressants)

Recurrent surgery

Severe illness

Trauma

Neurological disease (Parkinson’s, multiple sclerosis, Hirschsprung’s disease)

148
Q

How might pseudo-obstruction present

A

Abdominal pain

Abdominal distension

Constipation

Vomiting (late feature)

149
Q

What are the differentials for pseudo-obstruction

A

Mechanical obstruction

Paralytic ileus

Toxic megacolon

150
Q

What investigations are needed for pseudo-obstruction

A

Routine bloods

Abdominal X-ray (shows distension)

Abdominal CT (gold standard)

Motility studies

Consider biopsy

151
Q

What is the management for pseudo-obstruction

A

NBM

IV fluids

NG tube if vomiting

Usually recover in 24-48 hrs

Endoscopic decompression (insert flatus tube)

IV neostigmine (anticholinesterase)

Surgery: for perforation/ischaemia/not responding, segmental resection and anastomosis

152
Q

What is a volvulus

A

Twisting of loop of intestines around mesentery

Compromises bloods supply (get ischaemia, necrosis, perforation)

Mostly in sigmoid colon (longest mesentery)

153
Q

What are the risk factors for volvulus

A

Increasing age

Neuropsychiatric disorders

Nursing home residents

Chronic constipation

Chronic laxative use

M>F

Previous abdominal surgery

154
Q

How might volvulus present

A

Clinical features of bowel obstruction

Colicky pain

Abdominal distension

Absolute constipation

Vomiting (late sign)

Rapid onset

155
Q

What are the differentials for volvulus

A

Severe constipation

Pseudo-obstruction

Sigmoid diverticular disease

156
Q

What investigations are needed for volvulus

A

Routine bloods

CT abdo-pelvis (whirl sign)

Abdo X-ray (coffee-bean sign)

157
Q

What is the management for volvulus

A

Decompression by sigmoidoscopy

Insert flatus tube

Surgery (ischaemia, perforation, repeated failed decompressions, necrosis)

158
Q

What are the complications of volvulus

A

Bowel ischaemia

Perforation

Risk of recurrence

Complications of stoma

High mortality from surgery

159
Q

Give an overview of caecal volvulus

A

Bimodal age: 10-29, 60-79

Diagnosed via CT

Management: laparotomy and ileocaecal resection

160
Q

What are the 4 degrees of haemorrhoids

A

1st: remain in rectum

2nd: prolapse through anus on defecation, spontaneously reduce

3rd: prolapse through anus on defecation, need digital reduction

4th: remain persistently prolapsed

161
Q

What are the risk factors for haemorrhoids

A

Excessive straining

Increasing age

Raised intra-abdominal pressure

Pelvic/abdominal mass

Family history

Cardiac failure

Portal hypertension

162
Q

How might haemorrhoids present

A

Painless bright red PR bleeding

Itching

Rectal fullness

Anal lump

Soiling

Large can thrombose: painful

163
Q

What is the management for haemorrhoids

A

Lifestyle advice

Topical analgesia (lignocaine gel)

Rubber band ligation

Haemorrhoidal artery ligation

Haemorrhoidectomy

164
Q

What are the complications of haemorrhoids

A

Thrombosis

Ulceration

Gangrene

Skin tags

Perianal sepsis

165
Q

What is pilonidal sinus disease

A

Disease of inter-gluteal region

Formation of sinus in cleft of buttocks

Mostly males 16-30

166
Q

What is the pathophysiology of pilonidal sinus disease

A

Hair follicles in inter-gluteal cleft become infected and inflamed

Obstruction of follicle, extends inwards, forms pit

Foreign-body reaction causes formation of cavity

Connection of cavity to skin surface via epithelialised sinus tract

167
Q

What are the risk factors for pilonidal sinus disease

A

Caucasian males

Coarse dark body hair

Sitting for long periods

Increased sweating

Buttock friction

Obesity

Poor hygiene

Local trauma

168
Q

How might pilonidal sinus disease present

A

Mass in sacrococcygeal region

Intermittently red, painful, swollen

Discharge from sinus

Systemic features of infection

169
Q

What is the management for pilonidal sinus disease

A

Shave affected region

Wash sinus

Use antibiotics in septic episodes

Surgical: abscess incision, drainage and washout. In chronic disease, can remove pilonidal sinus tract (can leave open or do primary closure)

170
Q

What is perianal fistula

A

Abnormal connection between anal canal and perianal skin

Associated with anorectal abscess formation

171
Q

What are the risk factors for perianal fistula

A

Perianal abscess

Inflammatory bowel disease

Systemic disease (TB, diabetes, HIV)

History of trauma

Previous radiation therapy to anus

172
Q

How might perianal fistula present

A

Recurrent perianal abscesses

External opening of perineum

Fibrous tract underneath skin on DRE

173
Q

What is Park’c classification system for perianal fistula

A

Inter-sphincteric

Trans-sphincteric

Supra-sphincteric

Extra-sphincteric

174
Q

What investigations are needed for perianal fistula

A

Proctoscopy

MRI (for complex fistulas)

175
Q

What is the management for perianal fistula

A

Conservative

Surgical: fistulotomy (leave tract open), placement of seton (for high tract disease)

176
Q

What is the pathophysiology of anorectal abscess

A

Plugging of anal duct

Fluid stasis

Infection

177
Q

What are the categories of anorectal abscess

A

Perianal

Ischiorectal

Intersphincteric

Supralevator

178
Q

How might anorectal abscess present

A

Pain in perianal region

Worse on sitting down

Localised swelling

Itching

Discharge

Systemic features

Perianal mass

Surrounding cellulitis

179
Q

What is the management for anorectal abscess

A

Antibiotics

Analgesia

Incision and drainage (leave to heal by secondary intention)

180
Q

What is an anal fissure

A

Tear in mucosal lining of anal canal

Acute < 6 weeks

Chronic > 6 weeks

181
Q

What are the risk factors for anal fissure

A

Constipation

Dehydration

Inflammatory bowel disease

Chronic ischaemia

182
Q

How might anal fissure present

A

Intense pain on defecation

Bleeding

Itching

Visible fissure

DRE very painful (may need to examine under anaesthesia)

183
Q

What is the management for anal fissure

A

Laxatives

Analgesia

Topical anaesthetics

GTN/diltiazem cream (increase blood supply, relax internal anal sphincter)

Botox injections (relax internal anal sphincter)

Lateral sphincterotomy (division of internal sphincter)

184
Q

What is rectal prolapse

A

Protrusion of mucosal or full-thickness layer of rectal tissue out of anus

Partial thickness: rectal mucosa protrudes out of anus (stretching of connective tissue)

Full thickness: rectal wall protrudes out of anus (a form of sliding hernia)

185
Q

What are the risk factors for rectal prolapse

A

Increasing age

F>M

Multiple vaginal deliveries

Straining

Anorexia

Previous traumatic vaginal delivery

186
Q

How might rectal prolapse present

A

Rectal mucus discharge

Faecal incontinence

PR bleeding

Visible ulceration

Rectal fullness

Tenesmus

Repeated defecations

187
Q

What is the management for rectal prolapse

A

Increase fibre and fluids

Banding

Surgery: perianal of abdominal approach

Surgery (7 decks)

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