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GENERAL SURGERY > Acute Abdominal Presentations > Flashcards

Acute Abdominal Presentations Flashcards

1
Q

what are the 3 main components of bile

A

cholesterol
phospolipids
bile pigments
- stored in the gallbladder

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2
Q

give 5 risk factors for gallstones

A

obesity
female
fertility
>40
family history

  • also pregnancy and oral contraceptives as oestrogen causes more cholesterole to be secreted into bile
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3
Q

describe the presentation of biliary colic

A

sudden ,dully, colicky
- RUQ pain but may radiate to epigastrium and/or back
- pain precipitated by consumption of fatty foods
- nausea/vomiting

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4
Q

describe the pathophysiology of biliary colic

A
  • gallbladder neck is occluded
  • fatty acids stimulate dudodenum endocrine cells to release CCK which stimulates contraction of gallbladder
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5
Q

what will patients presenting with acute cholecystitis report

A

constant pain in RUQ or epigastrium + associated signs of inflamm e.g. fever or lethargy

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6
Q

what might you find O/E of a pt w cholecystitis

A

tender RUQ
- +ve murphy’s sign: apply pressure to RUQ and ask pt to inspire
- halt in inspiration due to pain

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7
Q

give some ddx for RUQ pain

A
  • GORD
  • peptic ulceration
  • acute pancreatitis
  • IBD
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8
Q

what blood tests might be of importance in diagnosing gallstone disease

A
  • FBC/CRP: inflamm response
  • LFTS: biliary colic/cholecystisis = raised ALP but normal ALP and bilirubin
  • amylase: pancreatitis
  • urinalysis + pregnancy test to rule out renal or tubo-ovarian pathology
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9
Q

what is the 1st line investigation into suspected gallstone pathology

A

trans-abdominal ultrasound
- presence
- gallbladder wall thickness
- bile duct dilatation

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10
Q

what is the gold standard for imaging gallstones

A

MRCP - magnetic resonance cholangiopancretography
- can show potential defects in the biliary tree, sensitivity approaches 100%

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11
Q

what is the management plan for biliary colic

A

analgesia: regular paracetamol +/- NSAIDs +/- opiates

  • advise about lifestyle factors e.g. low fat diet, weight loss, inc exercise
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12
Q

what is the surgical treatment of biliary colic

A

laparoscopic cholecystectomy
- should be offered within 6 weeks of first presentation

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13
Q

what should patients with acute cholecystitis be started on

A

IV ABx e.g. co-amoxiclav +/- metronidazole
- concurrent analgesia + anti-emetics (ondansetron)

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14
Q

what surgical intervention in indicated for acute cholecystitis

A

laparoscopic cholecystectomy
- within 1 week of presentation but ideally within 72 hours

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15
Q

what can be done if a cholecystitis patient is not fit for surgery and is not responding to abx

A

percutaneous cholecystostomy to drain the infection

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16
Q

give 4 complications of cholecystitis

A
  • mirizzi syndrome
  • gallbladder empyema
  • chronic cholecystitis
  • bouveret’s syndrome & gallstone ileus
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17
Q

what is mirizzi syndrome

A
  • stone in Hartmanns pouch or in cystic duct can cause compression of the adjacent common hepatic duct
  • OBSTRUCTIVE JAUNDICE
  • confirm diagnosis by MRCP
  • manage with lap chole
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18
Q

what is bouveret’s syndrome and gallstone ileus

A

inflammation of the gallbladder (typically if recurrent) can cause a fistula to form between the gallbladder wall and the small = cholecystoduodenal fistula

  1. Bouveret’s Syndrome – a stone impacts in the proximal duodenum, causing a gastric outlet obstruction
  2. Gallstone Ileus – a stone impacts at the terminal ileum (the narrowest part of the small bowel), causing a small bowel obstruction
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19
Q

what organisms commonly cause cholecystitis/cholangitis

A

gram -ve bacili
E.Coli, Klebsiella, Enterococcus
(Gentamicin)

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20
Q

what is mesenteric adenitis and what might cause it

A

swollen lymph nodes in the membrane that connect the bowel to abdo wall
- typically from viral or bac infection, some types of cancer or IBD

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21
Q

what is neutropenic sepsis and what is it caused by

A

low levels of neutrophils (WCC<2)
- gram +ve pathogens e.g. staph aureus, strep pneumoniae
- HIV, hepatitis, TB, sepsis, Lyme disease

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22
Q

what is the pathophysiology of diverticula formation

A
  • aging bowel naturally becomes weaker over time
  • movement of stool in the lumen causes an increase in luminal pressure = outpouching of the mucosa through the weaker areas of the bowel wall
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23
Q

how does diverticulitis arise and what are its consequences

A

bacteria can overgrow within the outpouchings = inflammation
- can perforate -> diffuse peritonitis, sepsis and death
- chronically can cause fistula formation (colovesical or colovaginal)

most commonly in the SIGMOID COLON

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24
Q

how does acute diverticulitis present

A
  • acute abdo pain LIF
  • sharp nature, worsened by movement
  • O/E: localised tenderness + systemic upset e.g. dec appetite, pyrexia, nausea
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25
Q

what factors might mask symptoms of diverticulitis

A

corticosteroids or immunosuppressants

26
Q

what are complications of diverticulitis

A
  • abscess
  • bleeding
  • strictures: scarred and fibrotic bowel –> LBO
  • fistulae
27
Q

how is a diverticular abscess managed

A

<5cm managed conservatively with IV ABX
- radiological drainage
- complicated multi-loculated abscess = surgical intervention via lap washout or Hartmann’s procedure

28
Q

what is the investigation of choice in suspected diverticulitis

A

CT abdomen-pelvis
- thickening of colonic wall
- pericolonic fat stranding
- abscess

do NOT perform colonoscopy as risk of perforation

29
Q

how is acute diverticulitis staged

A

Hinchey classification

30
Q

what is a Hartmann’s procedure

A

a sigmoid colectomy with formation of an end colostomy

31
Q

what should not be missed in a patient presenting with epigastric pain

A

MI!!! Request an ECG
- especially in diabetic patients with neuropathy as they will not feel the pain of an MI

32
Q

what are the 2 syndromes associated with cholangitis

A
  • charcots triad: RUQ, fever, jaundice
  • reynold’s pentad: jaundice, fever, RUQ, hypotension and confusion
33
Q

what is the immediate management of cholangitis

A

IV fluids + abx e.g. co-amox, metronidazole
- routine bloods + cultures

34
Q

what is the definitive management of cholangitis

A

endoscopic biliary decompression
- ERCP

35
Q

describe the pathophysiology of appendicitis

A

direct luminal obstruction usually a faecolith or lymphoid hyperplasia
- less commonly by a malignancy e.g. caecal adenocarcinoma or neuroendocrine tumour
- when obstructed, commensal bacteria multiply = acute inflamm
* reduced venous drainage + loc inflamm = inc pressure = ischaemia in appendiceal wall
- left untreated = necrosis - perforate

36
Q

what are risk factors of appendicitis

A
  • FHx
  • ethnicity: caucasians
  • environmental: seasonal presentation during summer
37
Q

what are the clinical features of appendicitis

A
  • dull peri-umbilical pain that is poorly localised (visceral) then migrates to right iliac fossa becoming sharp (parietal)
  • vomiting, anorexia, nausea, diarrhoea
  • O/E: rebound + percussion tenderness over McBurney’s point
  • severe: sepsis, tachycardia, hypotension and pyrexia
38
Q

what are specific signs of appendicitis

A
  • Rovsing’s sign: RIF pain on palpation of the LIF
  • psoas sign: RIF pain with extension of the R hip - retrocaecal appendix abutting the psoas muscle
39
Q

what are potential ddx for appendicitis

A
  • gynae: ovarian cyst rupture, ectopic pregnancy, PID
  • renal: ureteric stones, UTI
  • GI: IBD, Meckel’s
  • urological: testicular torison, epiddidymo-orchitis
40
Q

what are important differentials to consider in children presenting with suspected appendicitis

A
  • mesenteric adenitis
  • gastroenteritis
  • constipation
  • intussusception
  • UTI
41
Q

what investigations should be carried out in all patients with suspected appendicitis

A

urinalysis - assess for renal/urological cause
- pregnancy test in women of reproductive age (serum b-hCG)
- routine bloods

42
Q

what imaging should be carried out in all patients with suspected appendicitis

A
  • USS
  • CT: good sensitivity & specificity
  • MRI: 2nd line in children/pregnant women
43
Q

what is the definitive treatment for appendicitis

A

lap appendicectomy
- low risk
- allows direct visualisation of other organs
- sent to histo to assess for underlying malingnancy

44
Q

give 4 possible complications of acute appendicitis

A
  • perforation
  • surgical site infection
  • appendiceal mass
  • abscess formation
45
Q

what is an important differential for appendicitis in >35s that should not be missed

A

caecal cancer!
if >35 then do a CT scan to rule out

46
Q

give 4 causes of pain in the epigastric region

A
  • peptic ulcer disease
  • cholecystitis
  • pancreatitis
  • MI! - important to not miss, order ECG
47
Q

give 4 causes of pain in the peri-umbilical region

A
  • SBO & LBO
  • appendicitis
  • AAA
48
Q

what are the likely diagnoses of acute abdominal pain in those > 50

A
  • biliary tract disease
  • NSAP
  • appendicitis
  • bowel obstruction
49
Q

what are the likely diagnoses of acute abdominal pain in those < 50

A
  • NSAP
  • appendicitis
  • mesenteric adenitis
50
Q

what is pseudo-obstruction

A

a disorder characterised by dilatation of the colon due to an adynamic bowel in absence of mechanical obstruction

51
Q

where does pseudo-obstruction most commonly affect

A

caecum and descending colon

52
Q

explain the pathphysiology behind pseudo-obstruction

A

interruption of the autonomic nervous supply to the colon resulting in the absence of smooth muscle action in the bowel wall

53
Q

what can untreated pseudo-obstruction lead to

A

increasing colonic diameter –> inc risk of bowel ischaemia and bowel perforation

54
Q

give 4 possible causes of pseudo-obstruction

A
  • electrolyte imbalance or endocrine disorders e.g. hypercalcaemia
  • meds: opioids, CCBs, anti-depressants
  • recent surgery, severe systemic illness, trauma
  • neuro disease e.g. parkinson’s/MS
55
Q

what are the clinical features of pseudo-obstruction

A
  • abdo distension
  • abdo pain
  • absolute constipation
  • vomiting: often late due to distal location of the colon
  • O/E: distended & tympanic w absent bowel sounds
56
Q

what investigations should patients with suspected pseudo-obstruction undergo

A

routine bloods: FBC, U&Es, Ca2+/Mg2+ and thyroid function tests

57
Q

how can diagnosis of pseudo-obstruction be reached

A

CT abdo-pelvis + IV contrast: often entire colon is dilated w no obvious narrowing or transition point

  • AXR can be performed which will show evidence of bowel distension
58
Q

how can pseudo-obstruction and mechanical obstruction be differentiated

A

endoscopic assessment (flexible sigmoidoscopy)
- for firect visualisation and concurrent bowel decompression for symptomatic relief

59
Q

what is the management for pseudo-obstruction

A
  • aggressive fluid resus as they are often intravascularly fluid deplete
  • NGT if vomiting
  • urinary catheter for fluid balance assessment
  • adequate analgesia
  • correct electrolyte abnormalities
60
Q

what is the management for pseudo-obstruction that does not resolve within 24-48 hours

A

decompression by flexible sigmoidoscopy and insertion of a flatus tube is required
- if limited resolution can use IV neostigmine (anticholinesterase)
- but must be done in a high-dependency monitored setting due to side effects of severe bradycardia

61
Q

what is the management for pseudo-obstruction with evidence of bowel ischaemia or perforation

A

emergency surgery
- laparotomy + subtotal colectomy

GENERAL SURGERY (8 decks)

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