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Y4 final checklist_ SURGERY > Surgery conditions (2) > Flashcards

Surgery conditions (2) Flashcards

1
Q

Shoulder tip pain following a peritoneal perforation suggests irritation of where?

A

Diaphragm

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2
Q

What’s intussusception?

A

Intussusception ⇒ the invagination of one portion of bowel into the lumen of the adjacent bowel, most commonly around the ileo-caecal region

Intussusception usually affects infants between 6-18 months old.

Boys are affected twice as often as girls

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3
Q

Presentation/features of Intussusception

A
  • paroxysmal abdominal colic pain
  • during paroxysm the infant will characteristically draw their knees up and turn pale
  • vomiting
  • bloodstained stool - ‘red-currant jelly’ - is a late sign
  • sausage-shaped mass in the right upper quadrant
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4
Q

Ix for Intussusception (1)

A

ultrasound → may show a target-like mass

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6
Q

Management of intussusception

A
  • reduction by air insufflation under radiological control→ first-line
  • if this fails + signs of peritonitis → surgery
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7
Q

Possible cause of intussusception

A
  • Hypertrophied Peyer’s patch
  • Meckel’s
  • HSP
  • Peutz-Jeghers
  • Lymphoma
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8
Q

Does intussusception occur in adults?

A

Intussusception rarely occurs in an adult

• If it does, consider neoplasm as lead-point

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9
Q

What is the blood supply to the ascending colon?

A

Superior Mesenteric Artery

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10
Q

Causes of GI (gastro-intestinal) perforation

A

The most common: peptic ulcers (gastric or duodenal) and sigmoid diverticulum

  • Chemical
    • Peptic ulcer disease
    • Foreign body (e.g. battery or caustic soda)

​

  • Infection
    • Diverticulitis
    • Cholecystitis
    • Meckel’s Diverticulum
  • Ischaemia
    • Mesenteric ischaemia
    • Obstructing lesions → resulting in bowel distension and subsequent ischaemia and necrosis
  • Colitis
    • Toxic Megacolon (e.g. Clostridum Difficile or Ulcerative Colitis)
  • Iatrogenic
    • Recent surgery (including anastomotic leak)
    • Endoscopy or overzealous NG tube insertion
  • Penetrating or blunt trauma
    • Shear forces from acceleration-deceleration or high forces over small surface area (e.g. a handle bar)
  • Direct rupture
    • Excessive vomiting leading to oesophageal perforation (Boerhaave Syndrome)
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11
Q

Clinical features of GI perforation

A
  • pain → typically this is rapid onset and sharp in nature.
  • systemically unwell → may also have associated malaise, vomiting, and lethargy
  • features of sepsis
  • features of peritonism, which may be localised or generalized (a rigid abdomen)
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12
Q

Ix in GI perforation

A
  • ### routine baseline blood tests + G&S
  • WCC and CRP → commonly raised
  • amylase → often mildly elevated in perforation
  • urinalysis → to exclude both renal and tubo-ovarian pathology
  • erect chest radiograph (eCXR) can show free air under the diaphragm. Pneumomediastinum or widened mediastinum
  • CT scan → confirming any free air presence and suggesting a location of the perforation (as well as a possible underlying cause).
  • abdominal radiograph (AXR) → show signs of perforation
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13
Q

Signs of GI perforation on abdominal X ray

A
  • Rigler’s sign – both sides of the bowel wall can be seen, due to free intra-abdominal air acting as an additional contrast
  • Psoas sign – loss of the sharp delineation of the psoas muscle border, secondary to fluid in the retroperitoneum
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14
Q

Management of GI perforation (general)

A
  • Broad spectrum antibiotics should be started early, especially in patients
  • NIL and NG tube
  • IV fluid support
  • analgesia

Following this standard initial approach, management becomes highly individualised, taking into account the site of perforation and patient factors. However, most patients with a perforated viscus will require theatre for repair and control of contamination.

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15
Q

Key aspects to consider in surgical intervention for perforated GI (3)

A
  • Identification and (where possible) management of underlying cause
  • Appropriate management of perforation, such as:
    • Repairing perforated peptic ulcer with an omental patch
    • Resecting a perforated diverticulae (e.g. via a Hartmann’s procedure)
  • Thorough washout
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16
Q

In which groups of patients, should we consider conservative management of GI perforation?

A

Physiologically well patients may be managed conservatively, including patients with:

  • Localised diverticular abscess / perforation with only localised peritonitis and tenderness, and no evidence of generalised contamination on CT imaging
      • Patients with a sealed upper GI perforation on CT imaging without generalised peritonism
    • Elderly frail patients with extensive co-morbidities who would be very unlikely to survive surgery
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17
Q

Complications of GI perforation

A
  • infection (peritonitis and sepsis)
  • haemorrhage,
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18
Q

Surgical approach in perforation of stomach and duodenum

A
  • Any stomach or duodenum perforation can be accessed typically via an upper midline incision (also can be done laparoscopically), and a patch of omentum is tacked loosely over an ulcer which would otherwise be difficult to oversew due to tissue inflammation
  • All gastric ulcers should be biopsied to exclude malignancy
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19
Q

The surgical approach in perforation of small bowel

A
  • Small bowel perforations can be accessed via a midline laparotomy
  • small perforations can be oversewn if the bowel is viable, yet any doubt about the condition of bowel should lead to resection and primary anastomosis +/- stoma formation
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20
Q

Surgical approach to large bowel perforation

A
  • can be accessed via midline laparotomy
  • anastomosis in the presence of faecal contamination and an unstable patient is not recommended, so a resection with stoma formation is the preferred option
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21
Q

What’s GIST?

A

Gastro-Intestinal stromal tumour

  • Commonest mesenchymal tumour of the GIT
  • >50% occur in the stomach

Epidemiology

  • M=F
  • ~60yrs
  • ↑ with NF1
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22
Q

Pathophysiology of GIST

  • what cells
  • what is seen on OGD
A

GIST = gastro-intestinal stromal tumour

  • Arise from intestinal cells of Cajal
  • Located in muscularis propria
  • Pacemaker cells

• OGD: well-demarcated spherical mass with central

punctum

23
Q

Presentation of GIST (2)

A

GIST = gastro-intestinal stormal tumour

  • Mass effects: abdo pain, obstruction
  • Ulceration: → bleeding
24
Q

Management of GIST

A

GIST = gastro-intestinal stromal tumours

Medical

  • Unresectable, recurrent or metastatic disease
  • Imatinib: selective tyrosine kinase inhibitor

Surgical

  • Resection
25
Q

NHS screening for colorectal cancer: who, when and what?

A
  • screening every 2 years to all men and women aged 60 to 74 years in England
  • Patients aged over 74 years may request screening
  • eligible patients are sent Faecal Immunochemical Test (FIT) tests through the post
  • a type of faecal occult blood (FOB) test which uses antibodies that specifically recognise human haemoglobin (Hb)
  • used to detect, and can quantify, the amount of human blood in a single stool sample
  • a patient will be informed if the test is normal or abnormal
  • abnormal results → colonoscopy
26
(3) types of genetic colorectal cancer
* sporadic (95%) * hereditary non-polyposis colorectal carcinoma (HNPCC, 5%) * familial adenomatous polyposis (FAP, \<1%)
27
What's FAP?
**FAP = Familial Adenomatous Polyposis** * **autosomal dominant condition** * formation of **hundreds of polyps** by the age of 30-40 years * Patients inevitably develop carcinoma * mutation in a **tumour suppressor gene called adenomatous polyposis coli gene (APC),** located on chromosome 5
28
Management of FAP
**FAP = familial adenomatous polyposis** * Genetic testing →analysing DNA from a patient's white blood cells * Patients generally have a **total colectomy with ileo-anal pouch formation** in their 20s \*Patients with FAP are also at risk from duodenal tumours \*A variant of FAP called **Gardner's syndrome** → feature osteomas of the skull and mandible, retinal pigmentation, thyroid carcinoma and epidermoid cysts on the skin
29
**What's HNPCC?** Pathophysiology Cancers that are associated with HNPCC
**HNPCC = Hereditary Non-Polyposis Colorectar Carcinoma** * autosomal dominant condition * the most common form of inherited colon cancer * around 90% of patients develop cancers, often of the proximal colon, which are usually poorly differentiated and highly aggressive * mutations of DNA mismatch repair genes Higher risk of other cancers: endometrial cancer being the next most common association, after the colon
30
**Amsterdam's criteria** ## Footnote - what are they used for? - describe
Use: for HNPCC (Hereditary Non-Polyposis Colorectal Ca) The Amsterdam criteria → used to aid diagnosis: * at least 3 family members with colon cancer * the cases span at least two generations * at least one case diagnosed before the age of 50 years
31
Who to refer urgently for 2ww colorectal Ca service?
* patients \>= 40 years with unexplained weight loss AND abdominal pain * patients \>= 50 years with unexplained rectal bleeding * patients \>= 60 years with iron deficiency anaemia OR change in bowel habit * tests show occult blood in their faeces (see below)
32
Staging of colorectal cancer (3)
* Staging using **CT of the chest/ abdomen and pelvis** * entire colon → **colonoscopy** or **CT colonography** * If tumour lie below the peritoneal reflection → mesorectum MRI
33
Treatment of **colonic cancer**
* **Palliative adjuncts:** stents, surgical bypass and diversion stomas * **Resectional surgery** is the only option for cure * if an obstructing lesion→ either stent it or resect * **chemotherapy** (following resection) → a combination of 5FU and oxaliplatin is common
34
What does **resectional surgery for colonic cancer** involve?
The procedure is: * tailored to the patient and the tumour location * The lymphatic drainage of the colon follows the arterial supply and therefore most resections are tailored around the resection of particular lymphatic chains (e.g. ileo-colic pedicle for right sided tumours). * Confounding factors that will govern the choice of procedure: HNPCC family may be better served with a **panproctocolectomy** rather than segmental resection.
35
(2) techniques of surgical resection in **rectal cancer**
* anterior resection * abdomino-perineal excision of rectum (APER)
36
When **APER** is chosen as a surgical resection technique for **rectal cancer**? (2)
**APER = abdominoperineal excision of the rectum** * the involvement of the sphincter complex OR * very low tumours
37
Most common type of colorectal cancer
95% **adenocarcinoma** \*Others: lymphoma, GIST, carcinoid
38
Risk factors/ associations with colorectal ca
* Diet: ↓ fibre + ↑ animal fat / protein * IBD: CRC in 15% c¯ pancolitis for 20yrs * Familial: FAP, HNPCC, Peutz-Jeghers * Smoking * Genetics - No relative: 1/50 CRC risk - One 1st degree: 1/10
39
Presentation of colorectal cancer * Left-located * Right-located
**Left** * Altered bowel habit * PR mass (60%) * Obstruction (25%) * Bleeding / mucus PR * Tenesmus **Right** * Anaemia * Wt. loss * Abdominal pain **Either** * Abdominal mass * Perforation * Haemorrhage * Fistula
40
Clinical examination of a patient with suspected colorectal ca (possible findings)
* Palpable mass: per abdomen or PR * Perianal fistulae * Hepatomegaly * Anaemia * Signs of obstruction
41
Investigations for colorectal ca
**Bloods** * FBC: Hb * LFTs: mets * Tumour Marker: CEA (carcinoembryonic Ag) **Imaging** * CXR: lung mets * US liver: mets * CT and MRI **Staging** **•MRI** best for rectal Ca and liver mets • **Endoscopy + Biopsy** **•Colonoscopy**
42
**Duke** staging for Colorectal ca (components)
43
TMN staging for **colorectal ca**
44
What does the **grading of ca** depend on?
Grading from low to high * Based on cell morphology * Dysplasia, mitotic index, hyperchromatism
45
What's **Gardener's syndrome**?
Gardener’s (TODE) * **T**hyroid tumours * **O**steomas of the mandible, skull and long bones * **D**ental abnormalities: supernumerary teeth * **E**pidermal cysts
46
Peutz-Jeghers syndrome genetics
**Peutz-Jeghers Syndrome** * Autosomal dominant * STK11 mutation
47
Presentation and risks associated with Peutz-Jeghers syndrome
Presentation at 10-15yrs: • Mucocutaneous hyperpigmentation (macules on palms, buccal mucosa) • Multiple GI hamartomatous polyps (Intussusception, Haemorrhage) Cancer risks: * CRC, pancreas, breast, lung, ovaries, uterus
48
What are **inflammatory pseudopolyps**?
Regenerating islands of mucosa in UC
49
What are **hyperplastic polyps**?
* Piling up of goblet cells and absorptive cells * Serrated surface architecture * No malignant potential
50
What are **Hamartomatous polyps**?
* Tumour-like growths composed of tissues present at site where they develop * Sporadic or part of familial syndromes * Juvenile polyp: solitary hamartoma in children → “Cherry on a stalk”
51
**Juvenile Polyposis** - genetics - number of polyps - risk
**Juvenile Polyposis** * Autosomal dominant * \>10 hamartomatous polyps * ↑ CRC risk: need surveillance and polypectomy
52
What's **Cowden Syndrome**?
* Auto dominant * Macrocephaly + skin stigmata * Intestinal hamartomas * ↑ risk of extra-intestinal Ca

Y4 final checklist_ SURGERY (25 decks)

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