6 - Lower GI Flashcards

1
Q

What are the different classifications of inguinal hernias?

A

Hernias are a protrusion of part or all of an organ through the wall of the cavity that normally contains it

Direct Inguinal (20%) - Go through weakness in Hesselbach’s triangle. More common in older patients due to weaker abdominal wall or increased intrabdominal pressure

Indirect Inguinal (80%) - Bowel goes through inguinal canal through deep ring. Due to incomplete closure of processus vaginalis so congenital in origin

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2
Q

What are some risk factors for an inguinal hernia and what are the differential diagnoses?

A

Risk factors: male, increasing age, raised intraabdominal presure (chronic cough, heavy lifting, chronic constipation), obesity

Differentials: femoral hernia, saphena varix, inguinal lymphadenopathy, lipoma, internal iliac aneurysm, groin abscess, hydrocele

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3
Q

What are the clinical features of an inguinal hernia and how can you distinguish between a direct and indirect hernia?

A
  • Lump in the groin that may reduce when lying down and gets worse on standing
  • If incarcerated can be tender, swollen, irreducible and erythematous and can have signs of bowel obstruction. Pain out of proportion to clinical signs
  • Reduce hernia and put pressure over deep inguinal ring (mid point of inguinal ligament). Ask to cough, if protrudes this is direct, if not this is indirect. Confirmed on surgery cannot be relied on
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4
Q

When a patient presents with a groin lump (suspected inguinal hernia), what are some things you should do on examination?

A
  • Cough impulse
  • Location (superomedial is inguinal, inferolateral is femoral)
  • Reducible on lying down or with pressure
  • Does it go into scrotum (can you get above it, is it separate from the testes)
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5
Q

How are inguinal hernias diagnosed?

A

- Usually clincial

  • Only image if diagnostic uncertainty and give US in outpatient setting
  • If incarcerated/strangulated use CT
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6
Q

How are inguinal hernias managed generally?

A

- If strangulated: urgent surgical exploration (specific management varies)

- If symptomatic: offer surgical intervention due to risk of strangulation

- If asymptomatic: conservative but discuss risks of strangulation

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7
Q

How are symptomatic non-strangulated inguinal hernias surgically treated?

A

- Open Mesh Repair (Lichtenstein Technique): if unilateral

- Laparoscopic: for bilateral or recurrent inguinal hernias or can be used for primary hernia but high risk of chronic pain or females

Laparoscopic is a longer operating time but quicker post op recovery, fewer complications and less post-op pain

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8
Q

What type of patients are at high risk of chronic pain with an open inguinal mesh repair?

A
  • Young and active
  • Previous chronic pain
  • Predominant symptom of pain
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9
Q

What are the complications of inguinal hernias and post-operative complications for their repair?

A

Inguinal Hernia: incarceration, obstruction, strangulation

Post op: (see image)

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10
Q

What is the femoral canal made up of?

A

In the anterior thigh and contains lymph vessels, lymph nodes and loose connective tissue

Superior border is the femoral ring that is normal covered by a septum but some omentum or abdominal contents can get through and cause a hernia

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11
Q

What are some risk factors for a femoral hernia and why are they a high risk of strangulation?

A

- Risk Factors: female, pregnancy, raised intraabdominal pressure, increasing age

  • More prone to incarcerate as narrow neck and rigid borders of femoral canal with concave lacunar ligament
  • More common in women because of the wider anatomy of the pelvis
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12
Q

What are the clinical features of a femoral hernia?

A
  • Small lump in the groin medial to femoral pulse
  • Will present as emergency
  • Vomiting
  • Often irreducible due to tightness of femoral ring

Sometimes femoral hernia can roll above inguinal ligament and appear as inguinal hernia

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13
Q

What are some differential diagnoses for a femoral hernia?

A
  • Inguinal hernia
  • Femoral canal lipoma
  • Lymph node
  • Saphena varix (will disappear on lying and have palpable thrill)
  • Athletic pubalgia
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14
Q

How are femoral hernias investigated?

A
  • Clinical diagnosis
  • Pre-op assessment as will need surgery
  • Can do US or CT abdomen pelvis
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15
Q

How are femoral hernias managed?

A

- Surgery within 2 weeks of presentation due to risk of strangulation

  • Operation involves reducing hernia and reducing size of femoral ring by suture pectineal and inguinal ligaments or putting in mesh plug

- High or Low approach (Inguinal ligament). Low less likely to damage inguinal structures but less space to remove any compromised bowel. High approach used in emergency

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16
Q

What are the complications with femoral hernias and complications with their surgical repair?

A
  • Strangulation
  • Obstruction
  • Bowel resection if strangulation
  • Wound infection
  • Cardiorespiratory complications
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17
Q

What is an epigastric hernia and what causes them?

A
  • Occurs in the upper midline through the line albea
  • Usually due to raised chronic intraabdominal pressure (obesity, pregnancy, ascites)
  • Usually affect men and often asymptomatic
  • Midline mass that disappears on lying back
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18
Q

How can you distinguish between divarication of the recti and an epigastric hernia?

A

.

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19
Q

What is a paraumbilical hernia and how do they present?

A

Herniation through the linea alba around the umbilical region (not the actual umbilicus).

Due to chronic raised intraabdominal pressure and they have a lump around the umbilical region

Extremely common and often contain pre-peritoneal fat and sometimes bowel but rarely strangulate

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20
Q

What is a spigelian hernia?

A
  • Hernia that occurs at the semilunar line around the level of the arcuate line (lateral border of the rectus where the aponeuroses fuse)
  • Small tender mass at the lower lateral edge of the rectus abdominis
  • High risk of strangulation so urgent surgical repair
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21
Q

What is an obturator hernia and how will they present?

A
  • Hernia of the pelvic floor through the obturator foramen into the obturator canal
  • Common in elderly women who have lost a lot of weight

- Mass in upper medial thigh and may have features of bowel obstrution

  • May have positive Howship-Romberg sign due to compression of obturator nerve
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22
Q

What are Littre and Lumbar hernias?

A

Littre: herniation of a Meckels diverticulum, often into inguinal canal and often becomes strangulated

Lumbar: posterior hernia that occurs spontaneously or iatrogenically, posterior mass with back pain

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23
Q

What is a Richter’s hernia?

A

Any hernia site but the anti-mesenteric border becomes strangulated so only part of the lumen of the bowel is in the hernial sac

Tender irreducible mass and obstruction symptoms

Urgent surgical intervention

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24
Q

What are the contents of the inguinal canal in males?

A
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25
Q

What is the definition of the following terms:

  • Diarrhoea
  • Acute and Chronic diarrhoea
  • Dysentry
  • Traveller’s diarrhoea
A

Risk factors are poor food preparation, immunocompromised and poor personal hygeine

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26
Q

How can you tell what causative organism caused gastroenteritis?

A

Time between ingestion of food and symptoms

Bacterial toxins = hours

Virus = days

Bacteria = weeks

Parasites = months

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27
Q

What are the presenting features of gastroenteritis and what are some questions you should ask in the history of a patient presenting with this?

A
  • Cramp-like abdominal pain and diarrhoea (with possible mucus and blood)
  • May have vomiting, night sweats and weight loss
  • May have pyrexia and dehydration
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28
Q

How is gastroenteritis investigated and managed?

A

Ix: none unless blood/mucus in stool, immunocompromised or persistent, then do a stool culture

Mx: rehydration, education to prevent in the future, exclusion from work for 48 hours from last episode of D+V, if food posioning report as notifiable disease

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29
Q

What are some important causes of dysentry you should consider when a patient presents with gastroenteritis?

A
  • Campylobacter
  • Shigella
  • Salmonella
  • Norovirus
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30
Q

What are some viral infective causes of gastroenteritis?

A

- Norovirus: most common viral gastroenteritis in adults, usually abdominal cramps, D+V and lasts 1-3 days

- Rotavirus: common in young children and resolves in about a week

- Adenovirus: common in kids

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31
Q

What are some bacterial infective causes of gastroenteritis?

A
  • Campylobacter
  • Shigella
  • E.Coli
  • Salmonella

ALL GRAM NEGATIVE

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32
Q

What are some bacteria that produce toxins that cause gastroenteritis?

A

Usually acute onset D+V lasting 24 hours

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33
Q

What are some parasitic causes of gastroenteritis?

A

More common in traveller’s diarrhoea

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34
Q

What is the most common cause of hospital-acquired gastroenteritis and how does this organism cause symptoms?

A

C.Difficile (Gram-positive) usually arising following use of broad spectrum abx that disrupts normal microbiota so C.Diff can overgrow

Produces exotoxin A and B that cause an immune response from the bowel so inflammatory exudate on colonic mucosa

Severe bloody diarrhoea and risk of toxic megacolon (dilated bowel with risk of perforation)

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35
Q

How is C.Diff investigated and managed?

A

Ix: stool culture and C.Diff Toxin (CDT) testing

Mx: IV fluid rehydration, oral metronidazole (or vancomycin in severe cases)

Have low threshhold for treatment with immunocompromised patients regardless of the cause of the gastroenteritis

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36
Q

What are some non-infective causes of gastroenteritis?

A

- Radiation colitis

- IBD (Crohn’s and UC)

- Microscopic colitis

- Chronic ischaemic colitis (usually affects watershed area around splenic flexure and is seen on endoscopy as blue swollen mucosa)

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37
Q

What is the pathophysiology of angiodysplasia?

A

Causes GI bleeds and it caused by formation of arteriovenous malformations between previously healthy blood vessels, usually in caecum and ascending colon

Most common cause of small bowel bleeds and second most common cause of rectal bleeding in over 60s

Can be acquired or congenital

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38
Q

What are the clinical features of angiodysplasia and what are some differential diagnoses?

A

- Painless rectal bleeding AND

- Anaemia

  • If upper GI bleed melena and haematemesis
  • If lower GI haematochezia

- Differentials: oesophageal varices, GI malignancies, diverticular disease, coagulopathies

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39
Q

How is suspected angiodysplasia investigated?

A

Lab tests: blood tests including FBC, U+E’s, LFTs, clotting, G+S or crossmatch

Imaging: endoscopy or colonoscopy to rule out malignancy. may need capsule endoscopy if in small bowel. can do mesenteric angiography to plan for intervention

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40
Q

How is angiodysplasia managed?

A

Conservative

  • If haemodynamically stable

- Bed rest and IV fluids

  • Potential tranexamic acid

Radiographically

  • If persistent or severe

- Endoscopy that subjects bleeding vessel to argon and electrical current

- Mesenteric angiography for small bowel that cannot be reached on endoscopy. Embolisation of vessel after catheterisation

Surgically

- Bowel resection (high mortality so only do if necessary)

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41
Q

Patients with angiodysplasia are at risk of a major GI bleed, what are some risk factors associated with a poor outcome for a upper GI bleed?

A
  • Advancing age
  • Liver disease
  • Patient present in hypovolemic shock
  • Current inpatients
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42
Q

What are some complications of angiodysplasia treatment?

A

- Rebleeding post therapy

  • Risk of small bowel perforation in endoscopy
  • Risk of haematoma formation, arterial dissection, thrombosis and bowl ischaemia in mesenteric angiography
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43
Q

What are GEP-NETs and how are they classified?

A

Gastroenteropancreatic neuroendocrine tumours that originate from neuroendocrine cells in the tubular GI tract and pancreas and they have the potential to be malignant

Most located in small intestine, with the rest in the stomach and rectum

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44
Q

What are the risk factors for GEP-NETs?

A
  • Genetic
  • MEN1
  • VHL disease
  • Tuberous sclerosis complex (TSC)
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45
Q

How do GEP-NETs present?

A
  • Non-specific symptoms like vague abdominal pain, N+V, andominal distension
  • Unintentional weight loss
  • Can be functioning or non functioning depending on hormonal hypersecretion
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46
Q

How are GEP-NETs investigated?

A
  • Chromogranin A and 5-HIAA levels
  • Routine bloods including FBC, LFTs, pancreatic peptides
  • Genetic testing
  • Endoscopy or CT enterocylsis depending on location
  • If metastatic with unknown primary do whole body somatostatin receptor schintography SSRS
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47
Q

How are GEP-NETs managed?

A

Often palliative as metastatic on presentation

Poorly differentiated: surgical resection then chemo if localised or if metastatic just palliative chemo

Well differentiated: localised disease and any liver metastases should be resected

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48
Q

What is a carcinoid crisis?

A
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49
Q

What is the pathophysiology of appendicitis?

A

Usually affects people between aged 10-30

Usually due to luminal obstruction of appendix from a faecolith, lymphoid hyperplasia, impacted stool or rarely a tumour

When obstructed commensal bacteria in appendix multiply so acute inflammation. Reduced venous drainage and localised inflammation leads to increased pressure in the appendix and in turn ischaemia

If ischaemia untreated can lead to necrosis and then perforation

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50
Q

What are some risk factors for appendicitis and some differential diagnoses?

A

Risk factors: FHx, caucasian (but ethnic minorities more likely to perforate if get it), summer

Differentials: see image

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51
Q

What investigations are done if appendicitis is suspected?

A

Lab Tests: urinalysis to exclude UTI, serum b-hCG to exclude pregnancy, FBC to look for raised inflammatory markers and for pre-op assessment

Imaging: often not needed as clinical diagnosis but if uncertainty can do USS first line (especially for children as lower radiation) or CT

52
Q

How is appendicitis risk stratified?

A

Men: Appendicitis inflammatory response score

Women: Adult Appendicitis score

Children: Shera score

Helps to work out how probable the diagnosis is appendicitis

53
Q

How is appendicitis managed?

A

- Laparascopic appendectomy is gold standard

- If appendiceal mass give antibiotics then interval appendectomy 6-8 weeks later

  • After removal send to histology to rule out malignancy and then look around rest of abdomen to look for any other pathology and look for Meckel’s diverticulum
54
Q

What are some complications with appendicitis?

A

- Perforation and peritoneal contamination

- Surgical site infection

- Appendix mass where omentum and small bowel adhere to appendix

- Pelvic abscess with fever and palpable RIF mass that can be confirmed on CT then percutaneous drainage

55
Q

What are some clinical features of appendicitis and what features can you elicit on examination?

A

- Dull poorly localised peri-umbilical pain that migrates to RIF and is sharp and well localised

  • Can have vomiting, anorexia, nausea, constipation

- Rebound tenderness and percussion pain over McBurney’s point

- Guarding if perforated but this will also show tachycardia and hypotension

56
Q

How does acute appendicitis vary in children compared to adults?

A
  • Often present in atypical manner e.g diarrhoea, urinary symptoms, left sied pain
  • Always examine urinary, cardiorespiratory and genitals if male
  • Children under 6 who have had symptoms for over 48 hours more likely to have perforated
57
Q

What is the histology and aetiology of colorectal cancer?

A
  • Fourth most common cancer and second highest mortality
  • Mostly adenocarcinomas
  • Progression of normal mucosa to colonic adenoma (polyp) to invasive adenocarcinoma (adeno-carcinoma sequence)

- APC and HNPCC predisposes people to colorectal cancer

58
Q

What are some risk factors for colorectal cancer and what are some differential diagnoses?

A
  • 75% are sporadic with no risk factors
  • Increasing age
  • FHx
  • IBD
  • Low fibre diet
  • High processed meat intake
  • Smoking
  • High alcohol intake

Differentials: IBD and haemorrhoids

59
Q

What are the clinical features of colorectal cancer

A

Change in bowel habit, rectal bleeding, weight loss, abdominal pain, iron deficiency anaemia

Right sided: abdominal pain, occult bleeding/anaemia, mass in RIF, presents late

Left sided: PR bleeding, change in bowel habit, tenesmus, mass in LIF or on PR

60
Q

According to NICE guidelines, what patients should be sent for urgent investigations for suspected colorectal cancer?

A
  • ≥40yrs with unexplained weight loss and abdominal pain
  • ≥50yrs with unexplained rectal bleeding
  • ≥60yrs with iron‑deficiency anaemia or change in bowel habit
  • Positive occult blood screening test
61
Q

What investigations are done if colorectal cancer is suspected?

A

- FBC, LFTs, clotting (may show microcytic iron deficiency anaemia)

- CEA tumour marker to monitor disease progression

  • Gold standard is colonoscopy with biopsy
  • Once diagnosed stage with CT Chest/Abdo/Pelvis to look for metastases, can use MRI/Endo-anal US to assess any rectal cancers depth of invasion and suitability for trans-anal resection
62
Q

What staging system is used for colorectal cancer?

A

Duke’s Staging or TNM

63
Q

What are the different management options for colorectal cancer?

A

Only definitive cure is surgery

Surgical

Regional colectomy to ensure removal of primary tumour with adequate margins and lymphatic drainage followed by anastomosis or formation of stoma

Chemotherapy

  • Usually used adjuvantly in advanced disease
  • FOLFOX regime

Radiotherapy

  • Used in rectal cancer neoadjuvantly (if threatened circumferential resection on MRI) to shrink tumour to increase chance of complete resection
  • Not used in colon cancer due to risk of damage to small bowel

Palliative

- Endoluminal stenting to relieve acute bowel obstruction but risk of perforation, incontinence and migration and cannot be used in rectal as tenesmus

- Stoma formation to relieve same

  • Resection of metastases
64
Q

What are the different colonic resections used for colorectal cancer?

A

Right hemicolectomy: for caecal or ascending colon tumours. ileocolic, right colic and right branch of middle colic (SMA branches) are divide and removed

Left hemicolectomy: descending colon tumours. left branch of middle colic vessels, inferior mesenteric vein and left colic vessels divided

Sigmoidcolectomy: sigmoid colon tumours, IMA fully dissected out

Anterior resection: high rectal tumours >5cm from anus. favoured as leaves anal sphincter. often perform defunctioning loop ileostomy to protect anastomosis but can be reversed

Abdominoperineal Resection (AP): low rectal tumours <5cm from anus. Excision of distal colon, rectum and anal sphincters so needs permanent colostomy

65
Q

What is Hartmann’s procedure?

A

Used in emergency bowel surgery (e.g perf or obstruction)

Complete resection of recto-sigmoid colon with formation of end colostomy and closure of rectal stump.

Done when condition means primary anastomosis is not ideal

66
Q

What are the four different manifestations of diverticulum?

A

- Diverticulosis – the presence of diverticula (asymptomatic, incidental on imaging)

- Diverticular disease – symptoms arising from the diverticula

- Diverticulitis – inflammation of the diverticula

- Diverticular bleed – where the diverticulum erodes into a vessel and causes a large volume painless bleed

More common in men and developing countries

67
Q

What is the pathophysiology of diverticular disease?

A

Aging bowel becomes weakened and increase in intraluminal pressure from stool passing through causes outpouching of mucosa through weaker bits of bowel wall (the junctions between triangular muscles)

  • Bacteria can overgrow in outpouchings causing inflammation
  • In chronic cases fistula can form (colovesical and colovaginal)

- Simple or Complicated (abscess presence or free perforation)

68
Q

What are some risk factors and differentials for diverticular disease?

A

Risk factors: age, low fibre intake, obesity, smoking, FHx, NSAID use

Differentials: IBD, bowel cancer, mesenteric ischaemia, gynaecological causes, renal stones

69
Q

What are the clinical features of the following:

  • Diverticulosis
  • Diverticular disease
  • Acute diverticulitis
A

Diverticulosis: Asymptomatic found incidentally on imaging

Diverticular disease: Intermittent colicky lower abdominal pain that can be relieved by defecation. Altered bowel habit, nausea, flatulence

Acute diverticulitis: Acute sharp abdominal pain usually localised in LIF and worsened by movement. Localised tenderness and systemic symptoms e.g pyrexia, anorexia. If perforated signs of peritonitis

70
Q

What is important in a drug history when suspecting diverticulitis?

A

If taking corticosteroids or immunosuppressants can mask symptoms of diverticulitis even if perforated

Pain may be in lower right quadrant or suprapubic

71
Q

What is a diverticular abscess and how is it managed?

A

Complicated diverticulitis

Managed with IV antibiotics but if doesn’t get better do radiological drainage

If complicated multi-loculated abscess will need laparoscopic washout or Hartmann’s

72
Q

How is acute diverticulitis investigated?

A

Lab Tests: FBC, CRP, U+E’s, consider faecal calprotectin, G+S, venous blood gas, urine dipstick to rule out urological causes

Imaging: CT abdomen pelvis then flexible sigmoidoscopy or CT colonography

73
Q

Why should you not perform a colonoscopy with a suspected presentation of diverticulitis?

A

Increased risk of perforation

74
Q

How is acute diverticulitis staged?

A

Hinchey Classification based on CT findings helps clinical management

75
Q

How is diverticular disease managed?

A
  • Uncomplicated can be managed as outpatient with analgesia and fluid intake and arrange colonoscopy to exclude any masked malignancies
  • If diverticular bleed manage conservatively as often self-limiting
  • If significant bleed appropriate resuscitation with blood products, if fails embolisation or surgical resection
76
Q

How is acute diverticulitis managed?

A

Conservative: Abx, IV fluids, analgesia. Symptoms often improve after 2-3 days, if deterioraion repeat imaging to look for disease progression

Surgical (if perforation with faecal peritonitis or overwhelming sepsis): Hartmann’s procedure with reversal of colostomy at later date

77
Q

What are some complications of diverticular disease?

A

- High rate of recurrence: may opt for elective segmental resection

- Diverticular stricture: from repeated acute inflammation so bowel scarred and fibrotic. can cause large bowel obstruction, needs sigmoid colectomy

- Fistula formation: colovesical or colovaginal

78
Q

What antibiotics are used for acute diverticulitis?

A

5 days Co-amoxiclav or combination of cefalexin with metronidazole if allergic

Avoid NSAIDs and codeine due to risk of perforation

79
Q

What is the pathophysiology of Crohn’s disease?

A

Remitting and relapsing IBD with bimodal age distribution of 15-30 and then again at 60-80

Can affect any part of GI from mouth to anus but usually affects distal ileum and proximal colon.

Transmural inflammation with cobble stone appearance and skip lesions

80
Q

What is the aetiology of Crohn’s?

A

Unknown but family history, smoking, white european (Ashkenazi Jews) and appendicetomy all increase the risk of developing

81
Q

What are some of the differences between UC and Crohn’s?

A
  • Crohn’s has perianal disease but UC doesn’t
  • UC has bloody diarrhoea but Crohn’s doesn’t
  • UC continuous but Crohn’s is skip lesions
  • Smoking is protective for UC but risk factor for Crohn’s
82
Q

What are some clinical features of Crohn’s disease?

A
  • Episodic colicky abdominal pain and diarrhoea
  • Diarrhoea is chronic and can contain blood and mucus
  • Systemic malaise, anorexia and low grade fever
  • Malnourishment

- Oral aphthous ulcers

- Perianal disease

On examination look for abdominal tenderness, mouth or perianal lesions, signs of malabsorption/dehydration, extraintestinal manifestations

83
Q

What are some extra-intestinal features of Crohn’s?

A

- MSK: enteropathic arthritis and metabolic bone disease

- Skin: erythema nodosum and pyoderma gangrenosum

- Eyes: anterior uveitis, iritis

- HPB: PSC, cholangiocarcinoma, gallstones

- Renal: renal stones

84
Q

What are some investigations that can be done if you suspect Crohn’s?

A

Supportive

- Routine bloods: look for anaemia, low albumin due to malabsorption, raised inflammatory markers

- X-ray/CT in acute setting to rule out obstruction or toxic megacolon

- Faecal calprotectin and consider stool sample

Diagnostic

  • Gold standard colonoscopy with biopsy
  • CT abdomen pelvis
  • MRI to look for fistulae and perianal disease
  • Can do proctosigmoidoscopy under anaesthesia to examine and treat perianal fistula
85
Q

How is Crohn’s managed?

A

Acute attack: Fluid resus, nutritional support, prophylatic heparin and anti-embolic stockings as prothrombotic state when in IBD flare

Inducing remission: Corticosteroids and immunosuppressants like azathioprine. Can trial biologics like infliximab as rescue therapy

Maintaining remission: Azathioprine as monotherapy, can consider biologics if this fails or add in methotrexate. Smoking cessation. Colonoscopic surveillance due to risk of malignancy. Referred to IBD nurse specialist and offered enteral nutritional support

Surgical (when medical management fails, severe complications or growth impairment in younger pt): see image but as patients are high risk need to do preoperative optimisation. Take bowel-sparing aproach to avoid short gut syndrome

86
Q

What drug should you avoid in an acute attack of Crohn’s or UC and why?

A
  • Anti-motility drugs like loperamide as can precipitate toxic megacolon
  • Also avoid colonoscopy due to risk of perforation
  • Refer to gastroenterologist
87
Q

What are some of the complications of Crohn’s?

A

Gastrointestinal

  • Fistula
  • Stricture formation leading to bowel obstruction
  • Recurrent perianal abscesses and fistula
  • GI malignancy

Extraintestinal

  • Malabsorption and growth delay
  • Osteoporosis due to malabsorption and long term steroids
  • Increased risk of gallstones due to less bile salts reabsorbed in terminal ilium
  • Increase risk of renal stones due to malapsorption of fats so calcium stays in lumen but oxalate still absorbed freely so oxalate stones
88
Q

When should emergency surgery for Crohn’s be carried out?

A
  • Cases not responding to medical management
  • Bowel perforation
  • Toxic megacolon

Pay close attention to nutritional status!!!!

89
Q

What are the features of UC and the aetiology?

A

Remitting and relapsing disease that is usually in Caucasians with bimodal age distribution of 15-25 and then 66-65.

Unknown aetioloy but FHx and environmental triggers are risk factors. Smoking is protective factor

90
Q

What are the clinical features of UC?

A
  • Insidious onset of bloody diarrhoea

- PR bleeding and mucus discharge

  • Increased frequency and urgency of defecation

- Tenesmus

  • Abdominal pain
  • May have anorexia and low grade pyrexia

Clinical exam usually remarkable but if severe abdominal pain consider toxic megacolon and perforation

91
Q

How is the severity of a UC exacerbation graded?

A

Truelove and Witt Criteria

92
Q

What are some extra-intestinal manifestations of UC?

A

MSK: enteropathic arthritis or nail clubbing

Skin: erythema nodosum

Eyes: episcleritis, anterior uveitis, iritis

HPB: primary sclerosing cholangitis

93
Q

What are some differentials for UC?

A
  • Crohn’s (UC is more bloody stools)
  • Chronic infections (Schistosomiasis, Giardiasis, TB)
  • Mesenteric Ischaemia
  • Radiation colitis
  • Malignancy
  • IBS
  • Coeliacs
94
Q

What investigations should you do if you suspect UC?

A

Lab Tests: Routine bloods (FBC, U+Es, CRP, LFTs, clotting) to look for anaemia or deranged LFTs if acute flare, low albumin (malabsorption), raised CRP/ESR

Faecal Calprotectin and Stool Sample: Raised in IBD but not IBS and should be done on patients with recent onset lower GI symptoms

Imaging: Gold standard diagnostic is colonscopy with biopsy but avoid in acute exacerbation (sometimes flexi sig sufficient)

If acute flare do AXR or CT to assess for toxic megacolon and/or perforation

95
Q

If someone is having an acute flare of UC what will be seen on AXR?

A
  • Mural thickening and thumbprinting due to severe inflammation

- Lead pipe colon can be seen on barium studies with toxic megacolon

96
Q

How is UC managed?

A

Acute attack: Fluid resus, nutritional support, prophylatic heparin

Inducing remission: Corticosteroids and immunosuppressants e.g Sulfasalazine, with biologics trialled as rescue therapy, e.g Infliximab

Maintaining remission: Immunomodulators like sulfasalazine or biologics if first line fails. Colonoscopic surveillance due to risk of malignancy. IBD nurse specialist and enteral nutritional support

Surgical: around 30% will need this in their life, on another flashcard

97
Q

How is UC surgically managed?

A

- Total proctocolectomy with require ileostomy is curative

  • Some people go for subtotal colectomy and preserve the rectum

May need acute surgical treatment if refractory to medical management or toxic megacolon or bowel perforation or dysplastic cells found on routine monitoring so reduces risk of colonic carcinoma

98
Q

What are some complications of UC?

A

- Toxic megacolon (needs decompression of bowel ASAP due to high risk of perforation)

- Colorectal carcinoma

- Osteoporosis

- Pouchitis (abdominal pain, bloody diarrhoea, nausea that needs to be treated with metronidazole and ciprofloxacin)

99
Q

How does toxic megacolon present?

A

In IBD when bowel cannot get rid of air and faeces so dilates

  • Abdominal distension
  • Abdominal pain
  • Fever
  • Rapid heart rate
  • Shock
  • Guarding/rigidity
100
Q

What is the pathophysiology of a pseudoobstruction?

A

- Ogilvie syndrome: dilatation of the colon due to an adynamic bowel in the absence of a mechanical obstruction, often affects caecum and ascending colon

  • Thought to be due to interruption of the autonomic nervous supply resulting in absence of smooth muscle action
  • Can lead to toxic megacolon, bowel ischaemia, perforation
101
Q

What are the clinical features of a pseudoobstruction?

A
  • Abdominal pain and distension
  • Constipation
  • Late vomiting
  • On examination abdomen is distended, tympanic but soft and non-tender. If focal tenderness it is a sign of ischaemia so warning sign
102
Q

What are some investigations done when a pseudoobstruction is suspected?

A

- Blood tests: to assess for endocrine or biochemical causes e.g U+Es, Ca, Mg, TFTs

- AXR: only shows distension, cannot rule out mechanical obstruction

- Abdominal Pelvis with IV contrast: definitive diagnosis as can rule out mechanical obstruction and look at any complications

103
Q

How is a pseudoobstruction managed?

A

Conservative

  • Make patient NBM
  • Start IV fluids and fluid balance chart
  • If vomiting place NG tube to help decompression
  • If does not resolve in 24-48 hours insert flatus tube endoscopically
  • If above doesn’t work trial neostigmine
  • Consider nutritional support

Surgical (if non-responding or perforation)

  • If non responding but no perforation/iscaemia may need segmental resection +/- anastomosis
  • Can do caecostomy or ileostomy to decompress bowel long term
104
Q

What is the difference between a paralytic ileus and pseudoobstruction?

A

Pseudoobstruction is limited to colon and ileus is small and large bowel

105
Q

What is a volvulus and why does it cause issues?

A

Twisting a loop of intestine around its mesentry so there is a closed loop bowel obstruction

This compromises blood supply so leads to necrosis and perforation

Mostly occurs at sigmoid as has a long mesentry that gets bigger with age

106
Q

What are some risk factors for developing a volvulus?

A
  • Increasing age
  • Neuropsychiatric disorders
  • Live in nursing home
  • Chronic constipation or laxative use
  • Male
  • Previous abdominal operations
107
Q

What are some clinical features of a volvulus and what are some differentials?

A
  • Features of bowel obstruction

- Colicky pain, abdominal distension, absolute constipation

  • Compared to other bowel obstructions there is a faster onset and higher degree of abdominal distension
  • Abdomen tympanic to percussion
  • If signs of peforation or peritonism surgical emergency as this indicates ischaemia or perforation

Differentials: bowel obstruction, severe constipation, pseudoobstruction, sigmoid diverticular disease

108
Q

What are some investigations to do when a patient presents with a bowel obstructon potentially caused by volvulus?

A

- Routine bloods including electrolytes to rule out pseudo-obstruction

  • Initial CT abdomen pelvis with contrast. Will show very dilated sigmoid colon with ‘whirl sign’ due to twisting on mesentry
  • Can perform AXR and will have ‘coffee bean sign’ from LIF
109
Q

How is a sigmoid volvulus managed?

A

Conservative

- Rigid sigmoidoscopy with flatus tube insertion

Surgical

  • Laparotomy for Hartmann’s procedure
  • If recurrent volvulus may have elective sigmoidectomy to prevent further recurrence
110
Q

What are some complications of a sigmoid volvulus?

A
  • Bowel ischaemia and perforation
  • Risk of recurrence (90% of patients)
  • Complications from stoma if place

High mortality from surgery as often old and frail and has been a delay to getting them to surgery

111
Q

What is the aetiology of a caecal volvulus and how are they investigated and managed?

A
  • Second most common volvulus and occurs in bimodal age distribution age 10-29 (intestinal malformation and excessive exercise) and age 60-79 (chronic constipation, dementia, distal obstruction)

- CT imaging diagnosis with distended caecum and mesenteric swirl and small bowel obstruction

- Laparotomy and Ileocaecal resection always!!!!

112
Q

What are some common complications of appendicectomy?

A
113
Q

How long after an appendectomy can you go back to work and drive?

A
  • Can drive after 24 hours of anaesthetic if not taking strong painkillers but recommended not to drive for 2-4 weeks after laparoscopic and 4-6 weeks after open
  • Can return to work as soon as feeling well enough but can take 4-6 weeks. Avoid strenous activity and heavy lifting for 6 weeks
114
Q

What are some differentials for RUQ pain?

A
  • Acute cholecysitis
  • Pyelonephritis
  • Pneumonia
  • Hepatitis
  • Small bowel obstruction
115
Q

What is choledocholithiasis?

A

Gallstone in the CBD

116
Q

When should gallstones be operated on?

A

When they are symptomatic or risk of gallbladder cancer

117
Q

What are some differentials for LIF pain?

A
  • Diverticulitis
  • IBD
  • Ureteric colic
  • Testicular tumour
  • Inguinal hernia
  • UTI
  • PID
118
Q

What might you find on abdominal exam with diverticulitis?

A
  • Sharp pain in LIF that is worse on movement
  • Focal tenderness and/or guarding in LIF
  • May feel palpable mass in LIF
  • Decreased appetitie, nausea, pyrexia
  • If perforated will have signs of peritonitis (lying still)

BE CAREFUL IF PATIENT TAKING STEROIDS OR IMMUNOSUPPRESSANTS AS WILL MASK SYMPTOMS OF THIS AND PERFORATION

119
Q

What are the indications for surgery in IBD?

A
  • Perforation
  • Lack of improvement with medical management
  • Fulminant colitis
  • Massive hemorrhage
  • Haemodynamic instability
  • Fistulas and Abscesses
120
Q

Where are low and high risk geographical areas for diverticular disease?

A

Low: Africa and Asia

High: Western countries due to the lack of fibre

121
Q

What are some complications of diverticulitis and what are the indications for surgery?

A
  • Perforation
  • Diverticular strictures
  • Fistula formation
  • PR bleeding
  • Sepsis

Surgery when evidence of perforation, sepsis not responding to antibiotic therapy, or failure to improve despite conservative management

122
Q

What is a major risk when resecting a rectal tumour?

A

Risk of damaging superior hypogastric plexus so urinary and erectile issues

123
Q

What antibiotics are used to treat diverticulitis?

A

Co-amoxiclav and Metronidazole

124
Q

What is the advantage of a flexi sigmoidoscopy over colonoscopy?

A

Doesn’t need bowel preparation

125
Q

What investigations should you do when a patient presents with haemorrhoids?

A
  • Proctoscope to help grade haemorrhoid
  • >40 with new onset then flexible sigmoidoscopt as can be presentation of colon cancer
126
Q

How long off of work should someone have following an inguinal hernia repair?

A

Non-manual work after 2-3 weeks for open, or 1-2 weeks laparoscopic