Surgery - General Flashcards

1
Q

What are the most common causes of small and large bowel obstruction?

A
  • Most common small bowel causes = adhesions, hernia
  • Most common large bowel causes = malignancy, diverticular disease, volvulus
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2
Q

How does bowel obstruction present?

A
  • Presentation
    • Abdo pain (colicky or crampy)
    • Vomiting (early in proximal, late in distal)
    • Abdo distension
    • Absolute constipation (early in distal, late in proximal)
  • O/E
    • Surgical scars (adhesions etc), hernia, abdo distension
    • Assess fluid status
    • Tympanic on percussion
    • Tinkling bowel sounds on auscultation
    • Abdo tenderness (but if there is guarding/rebound tenderness then suspect ischaemia!!! Do vbg for lactate)
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3
Q

How would you investigate and manage bowel obstruction?

A
  • Investigations
    • Definitive = ct abdo pelvis with iv contrast
      • Differentiates between pseudo-obstruction and mechanical too
    • AXR
      • S bowel = dilated >3cm, central, valvulae conniventes (lines totally across bowel)
      • L bowel = dilated >6cm or >9cm in caecum, peripheral, haustra visible (incomplete lines across bowel)
      • In perforation you can see Riglers sign (both sides of bowel visible) or psoas sign (loss of sharp delineation of psoas muscle border)
    • Erect CXR if suspected bowel perf = pneumoperitoneum
  • Management
    • Conservative = “drip and suck”
      • NBM + NG tube to decompress bowel
      • IV fluids and correct electrolytes
      • Urinary catheter, fluids
      • Analgesia, anti-emetics
    • Adhesions = usually conservative unless strangulated/ischaemic
      • Do water soluble contrast study if not resolved in 24 hours
      • If contrast does not reach colon in 6 hours then take to theatre as it is unlikely to resolve
  • Surgical = generally a laparotomy, sometimes resection + stoma
    • For ischaemia or closed loop bowel obstruction
    • Or if patients treated conservatively don’t improve
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4
Q

What two ways does an upper GI bleed present as?

A

Melena (black tarry offensive smelling stools)

Haematemesis (vomiting blood)

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5
Q

What are some differentials for an upper GI bleed?

A
  • Peptic ulcer disease
    • Most signif bleeding if ulcer erodes through posterior gastric wall into gastroduodenal artery (also common in lesser curve of stomach)
    • Suspect in nsaids or steroids, dyspepsia like hx, h pylori positive
  • Variceal bleeds
    • Commonly Oesophageal varices due to alcoholic liver disease
  • Upper gi malignancy
  • oesophagitis
    • inflammation of intraluminal epithelial layer of the oesophagus
    • due to GORD (most common), or infections (candida albicans), meds (bisphosphonates), radiotherapy, crohns
  • Mallory Weiss tear
    • Recurrent vomiting then haematemesis
    • Forceful vomiting causes a tear in the epithelial lining of the oesophagus
  • Meckels diverticulum
  • Vascular malformations eg. dieulafoy lesion
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6
Q

How would you investigate an upper GI bleed generally?

+ scoring systems

A
  • Investigations
    • Oesophagogastroduodenoscopy is definitive
    • CT abdo with iv contrast to assess any active bleeding
    • Fbc, u&es, lfts, clotting, group and save, abg
    • Erect cxr if perforated peptic ulcer suspected
    • Glasgow-Blatchford Bleeding score for upper gi bleeds
    • Rockall severity score for GI bleeding post endoscopy
    • AIMS65 score for risk of in-hospital mortality from upper gi bleed
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7
Q

How would you manage an upper GI bleed generally?

(peptic ulcer and varices too)

A
  • Peptic ulcer
    • During OGD, give adrenaline injection** and **cauterise bleeding.
    • High dose ppi eg. iv 40mg omeprazole
    • Active bleeding can be treated with angio-embolisation
  • Oesophageal varices
    • Endoscopic banding
    • Prophylactic antibiotics
    • Somatostatin analogues (eg. octreotide) or vasopressors (eg terlipressin) to reduce splanchnic blood flow
    • Sengstaken-Blakemore tube for uncontrollable/severe
    • Longterm = repeated banding and long term BB
  • Blood products for hb<70g/L
  • FFP+/- platelets for impaired liver function
  • Reversal agents for anticoagulants
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8
Q

What are some differentials for a lower GI bleed?

A
  • Diverticular disease
    • Outpouchings of bowel wall consisting of mucosa
    • Commonly in descending and sigmoid colon
    • Diverticular disease bleeds are painless
    • Diverticulitis bleeds are painful
  • Ischaemic/infective colitis
  • Haemorrhoids
    • Engorged vascular cushions in anal canal
    • Blood on surface of stool not mixed
  • Malignancy
    • In elderly, always suspect colorectal cancer
  • Angiodysplasia
  • Crohns
  • UC
  • Radiation proctitis
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9
Q

How would you investigate and manage a lower GI bleed? and scoring systems

A

Investigations

  • Oakland score (stratifies if pt with lower gi bleed can be managed as outpatient)
  • Fbc,u&es, lfts, clotting, group and save, stool cultures
  • Urgent ct angiogram for haemodynamically unstable (can embolise during)
  • Flexi sigmoidoscopy
    • Full colonoscopy if nothing on flexi sig
    • OGD if nothing on colonoscopy
    • Capsule endoscopy or mri small bowel can also be done

Management

  • A-e resus
  • Packed rbc for hb<70, reverse anticoagulation
  • Endoscopic haemostasis methods eg. adrenaline injection
  • surgical
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10
Q

What are risk factors of GORD?

A
  • male, old age, obesity, alcohol, smoking, caffeine, spicy food
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11
Q

How dose GORD present?

A
  • Burning retrosternal chest pain (worse after meals, lying down, bending over, straining)
    • Relieved by antacids
  • Excessive burping
  • Odynophagia
  • chronic/nocturnal cough
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12
Q

How would you investigate and manage GORD?

A

Investigations

  • Los Angeles classification of reflux oesophagitis
  • OGD to rule out red flags for upper gi malignancy
    • Dysphagia
    • >55 with weight loss, upper abdo pain, dyspepsia, reflux
  • OGD also investigates oesophagitis, structuring, barretts
  • Gold standard for GORD = 24 hour pH monitoring
  • Oesophageal manometry to rule out oesophageal dysmotility

Management

  • Conservative
    • Avoid alcohol, coffee, fatty foods
    • Weight loss
    • Smoking cessation
    • PPIs
  • Surgical
    • Fundoplication (se = bloating, dysphagia, inability to vomit)
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13
Q

What are the two kinds of oesophageal cancer?

How would they present?

A

Squamous cell = middle and upper 1/3 of oesophagus

  • Risk factors = smoking, alcohol, low vit a, chronic achalasia

Adenocarcinoma = lower 1/3 of oesophagus

  • Risk factors = barretts (metaplastic epithelium that progresses to dysplasia), GORD, obesity, high fat intake

Presentation

  • Progressive dysphagia (solids first)
  • Weight loss, cachexia, supraclavicular lymphadenopathy
  • Odynophagia
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14
Q

How would you investigate and manage oesophageal cancer?

A

Investigations

  • Urgent OGD in 2weeks
    • Biopsy and send to histology
  • CT CAP and PET CT for mets
  • Endoscopic US to assess penetration into oesophageal wall (T stage)
  • Staging laparoscopy for intraperitoneal mets
  • Fine needle aspiration of palpable cervical lymph nodes
  • Bronchoscopy for hoarseness or haemoptysis

Management

  • Definitive
    • SCC = difficult to operate on so usually chemoradiotherapy
    • Adenocarcinoma = neoadjuvant chemo or chemoradiotherapy, followed by oesophageal resection
    • Most will need a feeding jejunostomy after surgery to aid nutrition
    • Surgery risks = anastomotic leak, pneumonia etc
  • Palliative
    • Oesophageal stent for difficulty swallowing
    • Radiotherapy/chemotherapy to reduce tumour size/bleeding
    • Nutritional support = thickened fluid and nutritional supplements
    • Radiological inserted gastrostomy (RIG) tube insertion for severe dysphagia
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15
Q

Oesophageal tears:

Boerhaave’s Syndrome is full thickness, Mallory Weiss is lacerations of the mucosa.

How does Boerhaave’s present?

A
  • Stomach contents leak into mediastinum and pleural cavity
  • Severe inflammatory response and multi organ failure
  • Causes = iatrogenic like endoscopy or forceful vomiting
  • Presentation
    • Severe sudden onset retrosternal chest pain, resp distress, subcutaneous emphysema
    • Hx of severe vomiting and retching
    • Mackler’s triad = vomiting, chest pain, subcut emph
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16
Q

How would you investigate and manage Boerhaaves?

A

Investigations

  • Fbc, u&es, lfts, clotting
  • Definitive = urgent ct abdo pelvis with iv and oral contrast
  • Cxr for pneumomediastinum or intrathoracic air fluid levels
  • If high clinical suspicion, just do urgent endoscopy in theatre

Management

  • A-e resus
  • Surgical
    • Endoscopy to determine site of perf
    • Thoracotomy to Control leak and wash out chest
    • Do a contrast ct at 10 days before starting oral intake as leaking is common
    • Insert feeding jejunostomy in surgery for nutrition
  • Non operative (iatrogenic perfs usually more suitable as they are more stable)
    • Resus and transfer to icu/hdu
    • Antibiotics and antifungal cover
    • NBM for 1-2 weeks, ng tube insertion on drainage
    • Large bore chest drain insertion
    • TPN or feeding jejunostomy insertion
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17
Q

How would a Mallory Weiss tear present?

A
  • Typically at gastro-oeosphgeal junction
  • Presentation
    • Hx of profuse vomiting then short period of haematemesis
    • Usually fine unless clotting abnormalities or anti-coag drugs
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18
Q

What is Achalasia? How would it present?

A

Achalasia = failure of LOS to relax, progressive failure of contraction of proximal oesophageal smooth muscle

  • Due to progressive destruction of ganglion cells in the myenteric plexus

Presentation

  • Progressive dysphagia with solids and liquids
  • Regurgitation
  • Coughing especially at night
  • Chest pain
  • Weight loss
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19
Q

How would you investigate and manage Achalasia?

A

Investigations

  • Barium swallow
  • oesophageal manometry is gold standard for motility disorders
    • shows absence of oesophageal peristalsis, failure of relaxation of LOS, high resting LOS tone
  • urgent OGD to rule out oesophageal cancer

Management

  • Conservative
    • Sleeping on pillows
    • Eating slowly
    • Chewing food thoroughly
    • More fluids with meals
    • CCB or nitrates (temporary)
    • Botox injections in LOS by endoscopy (temporary)
  • Surgical
    • Endoscopic balloon dilation
    • Laparoscopic heller myotomy
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20
Q

What is diffuse oesophageal spasm?

How would it present

A

Diffuse oesophageal spasm = multi focal high amplitude contractions of the oesophagus

  • Due to dysfunction of oesophageal inhibitory nerves

Presentation

  • Severe dysphagia to solid and liquids
  • Central chest pain exacerbated by food
    • Responds to nitrates
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21
Q

How would you investigate and manage diffuse oesophageal spasm?

A

Investigations

  • Manometry shows repetitive, simultaneous and ineffective contractions of the oesophagus
  • Barium swallow can show corkscrew appearance

Management

  • Nitrates or CCB to relax smooth muscle
  • Pneumatic dilation
  • Myotomy for severe
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22
Q

What is a hiatus hernia and what are the two types?

A

Hernia = Protrusion of a whole or part of an organ through the wall of the cavity that contains it into an abnormal position

Hiatus hernia = protrusion of an organ from the abdo cavity into the thorax through the oesophageal hiatus (usually stomach)

  • They can be classified into sliding or rolling
    • Sliding = Gastro-oesophageal junction + abdo part of oesophagus + cardia of stomach slides up through diaphragmatic hiatus into the thorax
    • Rolling = upward moving of gastric fundus so it lies beside a normal GOJ, resulting in a “bubble” of stomach in the thorax
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23
Q

What are some risk factors of a hiatus hernia?

A
  • old age (loss of diaphgragmatic tone), increased abdo pressure (eg. coughing, obesity, pregnancy, ascites)
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24
Q

How would a hiatus hernia present?

A
  • Mainly asymptomatic
  • Reflux eg. burning epigastric pain worse on lying flat
  • Hiccups or palpitations (large hernias can irritate diaphragm or pericardial sac)
  • Swallowing difficulties (oesophageal stricture formation)
  • Vomiting and weightloss
  • Bleeding/anaemia (oesophageal ulceration)
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25
Q

How would you investigate and manage a hiatus hernia?

A

Investigations

  • OGD is gold standard

Management

  • PPI like omeprazole
  • Weight loss, smaller meal portions with low fat content, sleeping with head of bed raised
  • Smoking cessation, reduce alcohol
  • Surgery like cruroplasty or fundoplication
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26
Q

What are some complications of a hiatus hernia?

A
  • Rolling ones are prone to incarceration and strangulation
  • Gastric volvulus can occur and cause obstruction and tissue necrosis
    • Borchardt’s triad of severe epigastric pain, retching without vomiting, inability to pass an NG tube
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27
Q

What is peptic ulcer disease?

A
  • A break in the lining of the GI tract extending through to the muscularis mucosae
  • Most commonly in the lesser curvature of the proximal stomach or the first part of the duodenum
  • Normal protective mechanisms = hco3- ions and mucous secretion by the gi mucosa
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28
Q

What are some risk factors of peptic ulcer disease?

A
  • Hpylori, Nsaids, corticosteroids, physiological stress, head trauma, Zollinger Ellison syndrome
  • Hpylori
    • Produces urease to break down urea into co2 and ammonia (neutralises stomach acid to create an alkaline environment)
    • Sets off inflammatory response
  • Zollinger Ellison syndrome
    • Triad of severe peptic ulcer disease + gastric acid hypersecretion + gastrinoma
    • Characteristic finding is a fasting gastrin level of >1000pg/ml
    • Associated with Multiple Endocrine Neoplasia Type 1 syndrome
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29
Q

How does peptic ulcer disease present?

A
  • Retrosternal or epigastric pain
    • Gastric is worse on eating, duodenal is worse 2-4 hours after eating or even alleviated by eating
  • Nausea, bloating, post-prandial discomfort, early satiety
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30
Q

How would you investigate and manage peptic ulcer disease?

A

Investigations

  • Nice says to do an urgent ogd for people with…
    • New onset dysphagia
    • >55 years old with weight loss and upper abdo pain/reflux/dyspepsia
    • New dyspepsia not responding to ppi
  • Ogd usually for older pts or red flag symptoms.
    • Biopsy any peptic ulceration for histology and rapid urease test
  • Most young low risk pts just need Non invasive h pylori testing
    • Carbon 13 urea breath test
    • Serum antibodies to h pylori
    • Stool antigen test

Management

  • Conservative
    • Smoking cessation, weight loss, reduce alcohol
    • Stop nsaids
    • Start on PPI for 4-8 weeks then reassess
    • Triple therapy for hpylori +ve (PPI + oral amoxi + clarithro OR metronidazole for 7 days)
  • Surgery for Emergencies like perf or severe relapsing disease = partial gastrectomy or selective vagotomy
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31
Q

How would Gastric cancer present?

And some risk factors

A
  • Typically Adenocarcinomas
  • Risk factors = male, hypylori, old age, smoking, alcohol

Typically present really late

  • Dyspepsia
  • Dysphagia
  • Early satiety
  • Vomiting
  • Melaena
  • Epigastric mass, Anorexia, weight loss, anaemia in late stage
  • Troisier sign = palpable left supraclavicular node (Virchows)
32
Q

How would you investigate and manage a gastric cancer?

A

Investigations

  • OGD and biopsy for histology, CLO test and HER2/neu protein expression
  • CT CAP and staging laparoscopy

Management

  • Nutritional assessment and support
  • Peri-op chemo and surgery (gastrectomy of some sort)
    • SE of gastrectomy = anastomotic leak, dumping syndrome, vit b12 deficiency
  • Early t1 tumours may have endoscopic mucosal resection
  • Palliative for late presentation (chemo, stenting, supportive)
33
Q

How would Gastroenteritis typically present? What would you do to investigate? (just one test)

A

Presentation

  • Diarrhoea = 3 or more loose stools per day (WHO)
    • Acute <14 days, chronic >14 days
  • vomiting, night sweats, weight loss
  • Dehydration and pyrexia
  • crampy abdo pain
  • typical hx = affected fam or friends, hx of travel, antibiotics within 4 weeks (c diff)

Investigations

  • Stool culture
34
Q

What are some common viral and bacterial causes of gastroenteritits?

A

Viral = norovirus, rotavirus (kids), adenovirus (kids)

Bacterial

  • Campylobacter = G-ve bacillus
    • Food poisoning from chicken, eggs milk
    • Can result in reactive arthritis, GBS, HUS, TTP
  • EColi = G-ve bacillus
    • Most common cause of travellers diarrhoea
  • Salmonella = G-ve flagellated bacillus
    • Uncooked poultry or raw eggs
    • Bloody diarrhoea
  • Shigella = G-ve bacillus
    • Contaminated dairy or water
    • Bloody diarrhoea
35
Q

What are some common parasitic causes of gastroenteritis? How would you manage them?

A

Commonly travellers diarrhoea

  • Cryptosporidium
  • Entamoeba hystolytica = metronidazole
  • Giardia intestinalis = metronidazole
  • Schistosomas = praziquantel
36
Q

How does hospital acquired C.Difficile gastroenteritis occur?

A

Hospital acquired = C. difficile (G+ve)

  • Following broad spec antibiotics that disrupt normal microbiota in bowel
  • C diff overgrow and produce excess exotoxin A and B
  • Results in inflammatory response in colonic mucosa = severe bloody diarrhoea
  • Complications = toxic megacolon if untreated

Investigate with stool culture + Cdiff toxin testing

Manage with IV fluids and oral metronidazole

37
Q

What is an inguinal hernia? What are the two different types

A
  • When abdo cavity contents enter the inguinal canal
  • Most common hernia

Direct (20%) = bowel enters inguinal canal through Hesselbach’s triangle

  • Typically in older patients due to increased intra abdo pressure or abdo wall laxity
  • Medial to inferior epigastric vessels

Indirect (80%) = bowel enters inguinal canal via deep inguinal ring

  • Typically due to incomplete closure of processes vaginalis
  • Lateral to inferior epigastric vessels
38
Q

How would an inguinal hernia present?

A
  • Lump in the groin that disappears when lying down
  • Incarcerated hernia = painful, tender, erythematous
    • Signs of bowel obstruction if bowel lumen is blocked
    • Features of strangulation if blood supply is compromised
    • Strangulation = irreducible, tender, tense, pain out of proportion to signs
  • Inguinal hernias are superomedial to the pubic tubercle, femoral is inferolateral
39
Q

How would you investigate and manage an inguinal hernia?

A

Investigations

  • Ultrasound first line
  • Obstruction or strangulation = ct imaging

Management

  • Symptomatic is offered surgical intervention
    • Strangulation = urgent surgical exploration
    • Primary inguinal hernias = open mesh repairs (Lichenstein technique)
    • Bilateral or recurrent inguinal hernias, or younger active patients with PIH = laparoscopic approach
      • Mesh repair has a risk of chronic pain
  • Non symptomatic = conservative
40
Q

What are some complications of hernias? (3)

A

Incarceration = contents cannot return to original cavity

Obstruction = lumen of bowel is obstructed

Strangulation = compression of hernia has compromised its blood supply leading to ischaemia

41
Q

What is a femoral hernia? What are some risk factors?

A
  • Less common but really high rate of strangulation!!
    • Rigid borders of femoral ring eg. lacunar ligament
  • More common in women due to wider bony pelvis
  • abdominal visceral pass through femoral ring into potential space of femoral canal
  • Risks = female, pregnant, high intra abdo pressure, old age
42
Q

How does a femoral hernia present?

What are some differentials?

A
  • Small lump in groin (inferolateral to pubic tubercle, medial to femoral pulse)
    • Usually not reducible due to tight borders of femoral ring
  • Differentials = inguinal hernia, saphena varix, femoral artery aneurysm
    • Saphena varix will disappear when lying flat, palpable thrill when coughing, varicose veins
43
Q

How would you investigate and manage a femoral hernia?

A

Investigations

  • Ultrasound Or CT abdo pelvis (high strangulation risk)
  • Surgical exploration

Management

  • All are managed surgically within 2 weeks of presentation due to risk of strangulation
    • Reduce hernia and narrow femoral ring
44
Q

What are some other types of abodminal wall hernias? (5)

A

Epigastric hernias

  • Occurs in upper midline through fibres of linea alba
  • Due to chronic raised intra abdo pressure

Paraumbilical hernia

  • Through linea alba around umbilical region
  • Due to chronic raised intra abdo pressure

Spigelian hernia

  • At semilunar line around level of arcuate line

Obturator hernia

  • Hernia of pelvic floor through the obturator foramen into obturator canal
  • Mass in upper medial thigh and features of small bowel obstruction
  • compression of obturator nerve causes +ve howship-romberg sign

Richters hernia

  • Partial herniation of bowel where anti-mesenteric border becomes strangulated
  • Tender irreducible mass + obstruction
45
Q

What is angiodysplasia?

How would it present?

A
  • Arteriovenous malformations between previously healthy blood vessels
  • Commonly in caecum and ascending colon
  • Can be acquired or congenital

Presentation

  • 10% asymptomatic = diagnosed on colonoscopy
  • majority are Painless occult PR bleeding
  • 10-15% is acute haemorrhage
46
Q

How would you investigate and manage angiodysplasia?

A

Investigations

  • Group and save or crossmatch and other routine tests
  • Haematinics as some have iron def anaemia
  • Exclude malignancy with an OGD or colonoscopy
  • Wireless capsule endoscopy to identify small bowel bleeds
  • Mesenteric angiography to find location of bleed

Management

  • Minimal bleeding = bed rest, IV fluids, tranexamic acid
  • Severe bleeding where site is identified
    • 1st line = argon plasma coagulation + endoscopy
    • Mesenteric angiography for small bowel lesions that cannot be treated endoscopically
  • Last resort is surgical (only for severe life threatening bleeds with multiple lesions etc)
47
Q

Pathophysiology of appendicitis?

A
  • Inflammation of the appendix
  • Luminal obstruction (secondary to faecolith, stool, caecal tumour)
  • Commensal bacteria multiply and cause acute inflammation
  • Obstruction causes reduced venous drainage and localised inflammation, resulting in increased pressure in the appendix
  • This can result in ischaemia and necrosis = perforation
48
Q

How does appendicitis present?

A
  • Initially dull poorly localised periumbilical pain (visceral peritoneum inflammation)
    • Becomes well localised sharp RIF pain (parietal peritoneum inflammation)
  • Vomiting that comes on after the pain
  • Anorexia, nausea, diarrhoea or constipation
  • Rebound tenderness and percussion pain over McBurney’s point
  • Guarding (esp in perforation)
  • Severe = sepsis (hypotensive, tachy)
  • On examination =
    • Rovsings (RIF pain on LIF palpation)
    • Psoas (RIF pain on right hip ext)
  • Remember presentation can be atypical in kids and with boys check for testicular torsion or epididymitis too. Also rule out intussusception and acute mesenteric adenitis
49
Q

How would you investigate and manage appendicitis?

A

Investigations

  • Urinalysis to rule out renal/urological causes (uti, pyelo, stones, TT etc)
  • Pregnancy test for women +serum bhcg
  • Routine bloods (fbc, u&es, lfts, crp, esr, clotting)
  • Ultrasound or CT not very conclusive, typically clinical diagnosis
  • Risk stratification scores
    • Men = Appendicitis inflammatory response score
    • Women = adult appendicitis score
    • Children = Shera score

Manage

  • Laparoscopic appendectomy is gold standard
    • Send to histopathology for malignancy
  • Appendiceal mass (appendiceal abscess?) = antibiotics then interval appendectomy 6 weeks later
50
Q

What are the different stages of diverticular disease?

A

Diverticulum = outpouching of bowel wall commonly in sigmoid colon

Diverticulosis = presence of diverticula

Diverticular disease = symptomatic diverticula

Diverticulitis = inflammation of diverticula

Diverticular bleed = diverticulum erodes into a vessel and causes large vol painless bleeding

51
Q

What is the pathophysiology of diverticular disease?

A
  • Aging bowel walls becomes weak and stool moving through the lumen increases luminal pressure
  • Therefore outpouchings of mucosa will form through weaker areas of bowel (typically where blood vessels penetrate or at junctions of muscle sheets)
  • Bacteria can overgrow in the outpouchings = diverticulitis
  • This can then cause perforation = peritonitis, sepsis, death
52
Q

How does diverticulosis, diverticular disease and diverticulitis present?

A

Diverticulosis = Typically asymptomatic and incidentally found on routine colonoscopy

Diverticular disease

  • Intermittent colicky lower abdo pain, relieved by defecation
  • Altered bowel habit, nausea, flatulence
  • No systemic features

Diverticulitis

  • Acute sharp abdo pain localised to LIF, worsened by movement
  • Localised tenderness
  • Systemic features eg. decreased appetite, pyrexia, nausea
  • Perforation = localised peritonism or generalised peritonitis
  • People on corticosteroids or immunosuppressants may have atypical symptoms
  • Diverticular abscess can form as a complication (IV antibiotics +/- radiological drainage for big ones)
53
Q

How would you investigate and manage diverticular disease?

A

Investigations

  • Routine bloods
  • Faecal calprotectin to rule out differentials
  • Diverticulitis = group and save, VBG, urine dipstick
  • CT abdo pelvis for diverticulitis = thickened colonic wall, pericolonic fat stranding, abscesses, localised air bubbles, free air
    • Hinchey classification to stage acute diverticulitis (Based on CT findings)
  • Flexible sigmoidoscopy for diverticular disease
    • Do not do this in diverticulitis as can risk perf

Management

  • Diverticular disease
    • Outpatient management = simple analgesia and oral fluids
    • Outpatient colonoscopy to exclude malignancies
    • Diverticular bleeds can also be managed conservatively or else with embolization and surgical resection
  • Acute diverticulitis
    • Conservative = antibiotics, iv fluids, analgesia
    • Surgical = for perf with faecal peritonitis or overwhelming sepsis
      • Typically Hartmann’s procedure
54
Q

What are some complications of diverticular disease?

A
  • Recurrence
  • Diverticular stricture due to repeated inflammation
    • can cause large bowel obstruction (needs sigmoid colectomy)
  • Fistula due to repeated inflammation
    • Colovesical between bowel and bladder (recurrent utis, faeces in urine, pneumoturia)
    • Colovaginal between bowel and vagina (copious vag discharge, recurrent vag infections)
55
Q

Crohns and UC in GI MEDICINE Notes (compare)

A
56
Q

What is pseudo-obstruction or Ogilvie syndrome?

A
  • Dilation of the colon due to an adynamic bowel in the absence of mechanical obstruction
  • Due to interruption of autonomic nervous supply to colon resulting in absence of smooth muscle action

Presentation = abdo pain, distension, constipation, vomiting is a late sign

57
Q

What are some causes of ogilvie syndrome?

A
  • Electrolyte imbalance eg. hypercalcaemia, hypothyroid, hypomagnesium
  • Meds eg. opioids, CCB, antidepressants
  • Recent surgery, illness, trauma
  • Neuro eg. parkinsons, ms, hirschsprungs
58
Q

How would you investigate and manage ogilvie syndrome?

A

Investigations

  • Routine bloods, u&es, ca2+, mg2+, tfts
  • AXR for bowel distension (but will show similar to mechanical)
  • CT abdo pelvis with iv contrast will show dilation and exclude mechanical obstruction and assess for complications like perf

Management

  • Conservative
    • Treat underlying cause
    • NBM and iv fluids, ng if vomiting
    • Endoscopic decompression if not resolved in 48 hours
      • Involves insertion of flatus tube
      • If limited resolution, use iv neostigmine
    • Nutritional support and review
  • Surgery is sometimes required for non responding cases, perf or ischaemia
59
Q

Describe the blood supply to the gut?

A

Foregut (stomach, duodenum, biliary, liver, pancreas, spleen) = coeliac artery

Midgut (distal duodenum, 1st half of transverse colon) = superior mesenteric artery

Hindgut (2nd half of the transverse colon to rectum) = inferior mesenteric artery

60
Q

What is chronic mesenteric ischaemia?

How would it present?

A

Mesenteric ischaemia is the lack of bloodflow through the mesenteric vessels supplying the intestines = ischaemia.

Pathophysiology:

  • Narrowing of the mesenteric vessels due to atherosclerosis
  • Presentation is essentially like angina but with your abdo ie pain when the blood supply can’t keep up with demand

Presentation:

  • Central colicky abdo pain starting 30mins after eating
  • Weight loss due to food avoidance
  • Abdominal bruit on auscultation
61
Q

How would you diagnose and manage chronic mesenteric ischaemia?

A

Diagnosis = CT angiography

Management:

  • Reduce risk factors eg smoking, diabetes, htn, cholesterol
  • Secondary prevention eg statins, antiplatelets
  • Revascularisation
    • 1st line is endovascular like percutaneous mesenteric artery stenting
    • 2nd line is open surgery like endarterectomy
62
Q

How does acute mesenteric ischaemia occur?

How would that present?

A
  • Rapid blockage in blood flow through superior mesenteric artery due to a thrombus in the artery (either a thrombus or an embolus)
  • Risk factors eg. AF

Presentation:

  • Acute, non specific abdo pain
  • Pain is disproportionate to exam findings
  • Can go into shock, peritonitis, sepsis
  • Eventually ischaemia –> necrosis of bowel tissue –> perf
63
Q

How would you investigate and manage acute mesenteric ischaemia?

A

Investigations:

  • Contrast CT
  • Metabolic Acidosis
  • Raised Lactate

Management:

  • Remove necrotic bowel
  • Remove or bypass thrombus (open surgery or endovascular)
64
Q

What is a volvulus?

A
  • Twisting of intestine around its mesenteric attachment resulting in a closed loop bowel obstruction
  • Can compromise bowel supply and cause ischaemia, necrosis, perf
  • Typically in sigmoid colon due to long mesentery (increases with age).
    • Therefore this segment of bowel is more prone to twisting on its mesenteric base
  • Risk factors = old age, neuropsych disorders, nursing home resident, chronic constipation or laxative use, male, prev abdo operations
65
Q

How does a volvulus present?

A
  • Bowel obstruction= colicky pain, abdo distension, absolute constipation. Vomiting late
  • Onset is pretty rapid (over hours)
  • Abdo is tympanic to percussion
66
Q

How would you imvestigate and manage a volvulus?

A

Investigations

  • Routine bloods (incl ones to exclude pseudo-obstruction)
  • Ct abdo pelvis with contrast = whirl sign
  • AXR = coffee bean sign in LIF

Management

  • Conservative
    • decompression with sigmoidoscope and flatus tube insertion
    • monitor for ischaemia
    • fluid resus
  • Surgical = laparotomy for hartmanns
    • Indications = ischaemia or perf, repeated failed decompression, necrotic bowel on endoscopy
67
Q

What is a haemorrhoid and what are the different degrees?

A
  • Abnormal swellings or enlargements of the anal vascular cushions
  • There are 3 Anal vascular cushions that help maintain continence (3, 7, 11oclock positions)

Classification

  • 1st degree remain in rectum
  • 2nd degree = prolapse through anus on defecation but spontaneously reduces
  • 3rd degree = prolapse through anus on defecation but requires digital reduction
  • 4th degree = remains persistently prolapsed
68
Q

How do haemorrhoids present?

And some risk factors?

A

Risk factors = excessive straining (chronic constipation), old age, raised intra abdo pressure, portal hypertension

Presentation

  • Painless bright red rectal bleeding after defecation on paper or surface of stool
  • Pruritus, rectal fullness or anal lump, soiling
  • Large prolapsed haemorrhoids can thrombose = painful, purple/blue oedematous tense tender perianal mass
69
Q

How would you investigate and manage haemrrhoids?

A

Investigations

  • Proctoscopy
  • Routine bloods
  • Flexi sigmoidoscopy or colonoscopy to rule out malignancy

Management

  • Conservative
    • Increased fibre and fluid
    • laxatives if necessary
    • Topical analgesia (lignocaine gel)
  • Rubber band ligation for symptomatic 1st and 2nd degree haemorrhoids
  • Surgical
    • Haemorrhoidal artery ligation for 2nd or 3rd degree haemorrhoids
    • Haemorrhoidectomy for 3rd or 4th degree or symptomatic and not responding to conservative therapies
70
Q

What is an anorectal abscess? What are the different classifications?

A
  • Collection of pus in anal/rectal region due to plugging of anal ducts, resulting in fluid stasis and infection
    • Commonly ecoli, bacteriodes spp, enterococcus spp
  • Classified as perianal, ischiorectal, intersphincteric or supralevator
71
Q

How would an anorectal abscess present?

A
  • Pain in perianal region exacerbated by sitting
  • Localised swelling, itching, discharge
  • Severe abscess = systemic like fever, rigors, malaise, sepsis
  • O/E = erythematous fluctuant tender perianal mass
72
Q

How would you investigate and manage an anorectal abscess?

A

Investigations

  • DRE
  • Examination under anaesthesia
  • Some need ct or mri

Management

  • Antibiotic therapy and analgesia
  • Incision and drainage of abscess under GA
    • Heal by secondary intention
  • Proctoscopy afterwards to check for fistula-in-ano
    • Insert a seton if fistula is identified
73
Q

What is an anal fissure and some risk factors?

A
  • Tear in the mucosal lining of the anal canal typically due to trauma from hard stool defecation
  • Acute is <6 weeks, chronic is >6 weeks
  • Risk factors = constipation, dehydration, IBD, chronic diarrhoea
74
Q

How would an anal fissure present?

A
  • Intense pain post defecation
  • Bleeding (bright red on wiping) or itching post defecation
  • O/E fissures are visible and palpable on dre
    • Most fissures are on the posterior midline
    • Often DRE is too painful so do examination under anaesthesia
  • Fissures within anal canal can be seen with proctoscopy
75
Q

How would you manage an anal fissure?

A
  • Reduce risk factors = fluids, fibre, stool softening laxatives like Movicol or lactulose
  • Topical analgesia like lidocaine or hot baths
    • 2nd line is gtn cream or diltiazem cream

Surgery for chronic fissures where med has not worked

  • Botox injections into internal anal sphincter
  • Or lateral sphincterotomy
76
Q
A