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GI 1 Flashcards

1
Q

at what point does reflux of gastric contents into the oesophagus become GORD, instead of a normal occurrence?

A

when it begins to cause symptoms

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2
Q

what 3 problems might prolonged GORD cause?

A

oesophagitis, benign oesophageal strictures, Barrett’s oesophagus

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3
Q

give 3 causes of GORD

A

lower oesophageal sphicter hypotension, hiatus hernia, loss of oesophageal peristaltic function, abdominal obesity, gastric acid hypersecretion, slow gastric emptying

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4
Q

give 3 risk factors for GORD

A

overeating, smoking, alcohol, pregnancy, surgery in achalasia, drugs, systemic sclerosis

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5
Q

explain the pathophysiology of GORD

A

LOS tone reduced + frequent transient LOS relaxation.

increased mucosal sensitivity to gastric acid + reduced oesophageal clearance of acid.

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6
Q

describe the pain felt in GORD

A

burning pain, aggravated by lying flat/bending over and on drinking hot drinks/alcohol, after big meals - relieved by antacids.

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7
Q

give 2 features of GORD, apart from chest pain

A

belching, acid/bile regurgitation, increased saliva production, odynophage (painful swallowing)

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8
Q

give 2 extra-oesophageal features of GORD

A

nocturnal asthma, chronic cough, laryngitis (hoarseness, throat clearing), sinusitis

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9
Q

give 2 possible complications of GORD

A

oesophagitis, ulcers, benign stricture, iron-deficiency. Barrett’s oesophagus.

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10
Q

what is Barrett’s oesophagus? how does it put GORD patients at greater risk of oesophageal cancer?

A

distal oesophageal epithelium undergoes metaplasia from squamous to columnar.
metalplasia -> dyplasia -> neoplasia.
this pattern means those with low-grade Barrett’s oesophagus are more likely to progress to cancer.

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11
Q

give 3 differential diagnoses of GORD

A 
oesophagitis due to corrosives, NSAIDs, herpes, Candida.
duodenal/gastric ulcers or cancers.
non-ulcer dyspepsia.
sphincter of Oddi malfunction.
cardiac disease.
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12
Q

give 3 red flag features of upper GI diseases. what would you do if a patient had these?

A 
ALARM symptoms:
Anaemia (iron-deficiency)
Loss of weight.
Anorexia.
Recent onset/progressive symptoms.
Malaena/haematemesis.
Swallowing difficulty.

endoscopy to check for upper GI cancers.

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13
Q

describe the lifestyle changes you would advise a GORD patient to make

A

lose weight, avoid alcohol, hot drinks, citrus fruits, fizzy drinks, spicy foods etc.
smoking cessation.
raise bed head.
eat small regular meals, don’t eat close to bed time.

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14
Q

how might you manage GORD, beyond lifestyle changes?

A

antacids or alginates.
oesophagitis - PPIs (lansoprazole, omeprazole etc).
H2-receptor blockers (rantidine).
laprascopic surgery - increase LOS pressure.

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15
Q

how do alginates/antacids work?

A

usually given as compound preparations.
antacids buffer stomach acid.
alginates increase the viscosity of stomach contents.
they form a floating ‘raft’ separating gastric contents from the gastro-oesophageal junction.

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16
Q

how do PPIs work?

A

irreversibly inhibit gastric H+/K+-ATPase.
block luminal secretion of gastric acid.
by targeting this final stage of gastric acid production, they can suppress it almost completely - more effective than H2 receptor blockers.

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17
Q

how do H2 receptor antagonists work?

A

reduce gastric acid secretion. they block the H2 (histamine) receptors on the gastric parietal cell, preventing activation of the proton pump.
pump still stimulated by other pathways, so H2 receptor blockers are not as effective as PPIs.

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18
Q

what causes a Mallory-Weiss tear? how might it present

A

persistent vomiting/retching - causes haematemesis via an oesophageal mucosal tear.

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19
Q

what are Mallory-Weiss tears associated with?

A

alcoholism and eating disorders

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20
Q

what is a peptic ulcer? where do they usually occur?

A

an ulcer of the mucosa in/adjacent to an acid-bearing area.

stomach + proximal duodenum. - duodenum more common.

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21
Q

what two things cause most peptic ulcers?

A

H. pylori

NSAIDs/aspirin

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22
Q

list 3 risk factors for duodenal ulcers

A
  • H pylori
  • NSAIDs, steroids, SSRIs
    increased gastric acid secretion.
    increased gastric emptying (lowers duodenal pH).
    blood group O.
    smoking.
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23
Q

list 3 risk factors for gastric ulcers

A

H pylori, smoking, NSAIDs, reflux of duodenal contents, delayed gastric emptying

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24
Q

what are the differences between the epigastric pain of a gastric ulcer and of a duodenal ulcer?

A

gastric - worse with food, better when hungry.

duodenal - worse when hungry, better with food or milk.

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25
Q

give 2 features of peptic ulcer disease apart from epigastric pain

A

bloating, fullness after meals, heartburn, tender epigastrium.

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26
Q

what investigations would be carried out in peptic ulcer disease? what would you expect to see?

A

endoscopy - biopsy all ulcers to exclude malignancy.

C13-urea breath test for H pylori ± stool antigen test - immunoassay using monoclonal antibodies.

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27
Q

how would you treat an H pylori +ve peptic ulcer patient?

A

eradication regimens - omeprazole + metronidazole + clarithromycin.

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28
Q

how would you treat an H pylori -ve peptic ulcer patient?

A

stop aspirin/NSAIDs.

PPIs - lansoprazole (or rantidine - H2 blocker).

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29
Q

give 2 possible complications of peptic ulcer disease

A

perforation (surgical closure, drain abdo).
bleeding.
malignancy.
gastric outflow obstruction.

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30
Q

what group of patients is at highest risk of developing oesophageal varices? why?

A

cirrhosis patients - portal hypertension causes dilated collateral veins at site of portosystemic anastomoses

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31
Q

what is the complication risk with oesophageal varices?

A

that they will cause an acute haemorrhage - life-threatening.
the varices protrude into oesophageal lumen so are easily traumatised by passing food.

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32
Q

how would you manage a patient bleeding from oesophageal varices?

A

restore blood volume and correct clotting abnormalities - vit K.
endoscopic banding, sclerosing or cauterising.
vasocontrictors - terlipressin.

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33
Q

give 3 clinical features of achalasia

A

dysphagia for both solids and liquids.
regurgitation of food, esp at night.
chest pain due to oesophageal spasm.
weight loss.

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34
Q

what is achalasia?

A

oesophageal motility disorder - LOS fails to relax due to degeneration of the myenteric plexus.

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35
Q

explain the pathogenesis of achalasia

A

inflammation of myenteric plexus of the oesophagus with ganglion loss - causes loss of nitric oxide, so impaired relaxation of the LOS and oesophageal peristalsis

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36
Q

what might you find on barium swallow of a patient with achalasia?

A

lack of peristalsis and swan neck/beak deformity at lower oesophagus

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37
Q

what cosmetic drug might help a patient with achalasia?

A

botulinum toxin A (botox) - injected into LOS

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38
Q

what surgical treatments are available to treat achalasia?

A

endoscopic balloon dilation or Heller’s cardiomyotomy (surgical division of LOS)

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39
Q

what is the most common cause of gastritis?

A

H pylori

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40
Q

how do NSAIDs cause gastritis?

A

they inhibit the COX pathway - COX1 is involved in mucus production so there is a depletion of mucosal prostaglandins

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41
Q

explain the pathology of autoimmune gastritis

A

combination of atrophic gastritis and loss of parietal cells, which affects the fundus and body of the stomach. there are serum antibodies to gastric parietal cells, which can lead to pernicious anaemia.

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42
Q

what is gastritis?

A

inflammation of the gastric mucosa - histological diagnosis, usually an incidental finding on gastric mucosal biopsy

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43
Q

list 3 causes of gastritis

A

H pylori, NSAIDs, autoimmune, viruses, hiatus hernia, alcohol

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44
Q

how might gastritis present?

A

asymptomatic, or epigastric pain, vomiting, haematemesis

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45
Q

how would you treat gastritis?

A

ranitidine (H2 blocker) or PPI.

H pylori eradication if needed.

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46
Q

give 3 causes of malabsorption that are common in the UK

A

coeliac disease, chronic pancreatitis, crohn’s disease

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47
Q

give 3 rarer causes of malabsoprtion

A

decreased bile - primary biliary cirrhosis, ileal resection, biliary obstruction.
pancreatic insufficiency - pancreatic cancer, cystic fibrosis.
small bowel mucosa - Whipple’s disease, tropical sprue, small bowel resection.
infection - giardiasis, strongloidiasis.

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48
Q

what 3 signs would be seen on histology in coeliac disease?

A

crypt hyperplasia and villous atrophy + lymphocytic infiltration

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49
Q

what is coeliac disease?

A

gluten-sensitive enteropathy. T cell mediated autoimmune disease.
abnormal jejunal mucosa that improves when gluten is removed and relapses when gluten is reintroduced.

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50
Q

explain the pathogenesis of coeliac disease

A

HLA-DQ2/DQ8.
alpha gliadin passes through damaged epithelium of small intestine - deaminated by tissue transglutaminase.
interacts with APCs to activate T cells.
inflammation - leads to villous atrophy and crypt hyperplasia.

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51
Q

give 5 clinical features of coeliac disease

A

stinking, pale stools that are hard to flush (steatorrhoea).
diarrhoea, abdo pain, bloating, nausea/vomiting, aphthous ulcers, angular stomatitis, weight loss, fatigue, weakness, osteomalacia, failure to thrive.

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52
Q

list 3 differential diagnoses of coeliac disease

A

IBS, lactose/other food intolerances, IBDs, dermatitis herpetiformis, tropical sprue, bacterial overgrowth, intestinal resection, Whipple’s disease, radiation enteritis.

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53
Q

what 2 signs would you see on serology of a patient with coeliac disease?

A

low folate/iron, IgA anti-tissue transglutaminase antibodies, anti-enodmyseal antibodies (anti-EMA)

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54
Q

what is the gold standard investigation for coeliac disease?

A

small bowel biopsy by endoscopy

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55
Q

why would coeliac disease patients be advised to get regular vaccinations?

A

hyposplenism is common, making them more susceptible to infections

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56
Q

how would you manage coeliac disease?

A

life-long gluten free diet (must reintroduce gluten a couple of weeks before biopsies taken, but can be stopped initially as a way of identifying coeliac disease).
avoid - wheat, rye and barley.
gluten-free biscuits, flour, bread and pasta are prescribable.

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57
Q

give 2 possible complications of coeliac disease

A

anaemia, secondary lactose intolerance, increased risk of malignancy, osteoporosis

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58
Q

what is tropical sprue?

A

a progressive small intestinal disorder occurring in residents/visitors to endemic areas in tropics

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59
Q

describe the pathological features of tropical sprue

A

villous atrophy + malabsorption (esp. fat and vit B12)

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60
Q

how does tropical sprue present?

A

diarrhoea, steatorrhoea, megaloblastic anaemia

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61
Q

how would you treat tropical sprue?

A

tetracycline + folic acid and mineral supplements.

exclude coeliac disease and acute infective diarrhoea.

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62
Q

where in the GI tract might Crohn’s disease affect?

A

mouth to anus.

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63
Q

describe the lesions seen in Crohn’s disease

A

skip lesions - there are areas of unaffected bowel between areas of active disease.

there’s transmural inflammation (inflammation spanning full depth of wall) - causes ulceration of superficial mucosa, possibly granulomas

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64
Q

what would you see on endoscopy in Crohn’s disease?

A

cobblestone appearance - due to skip lesions of inflammation/ulceration and deep fissures.

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65
Q

give 3 symptoms of Crohn’s disease

A

diarrhoea/urgency.
abdo pain.
weight loss.
fever, malaise, anorexia.

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66
Q

give 3 signs of Crohn’s disease

A 
aphthous ulcers (in mouth).
abdo tenderness/mass.
perianal abscess/fistulas/anal strictures.

extra-GI - clubbing, conjunctivitis, peripheral arthropathies, erythema nodosum, fatty liver, renal stones.

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67
Q

list 3 possible complications of Crohn’s disease

A

small bowel obstruction, toxic megacolon, abscess formation, fistulae, perforation, colon cancer, fatty liver, PSC, renal stones, osteomalacia, malnutrition, amyloidosis

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68
Q

list 3 differential diagnoses of Crohn’s

A

UC.
TB, carcinoid syndrome, amyloidosis, infective diarrhoea, bowel carcinoma, ischaemic colitis, diverticulitis, coeliac disease, IBS

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69
Q

what investigation would you carry out to confirm a diagnosis of Crohn’s disease?

A

endoscopy/colonoscopy with multiple biopsies for histology

70
Q

how would you manage Crohn’s?

A

oral steroids - prednisolone, hyrdocortisone.

control diarrhoea with loperamide.

71
Q

describe the surgical management of Crohn’s disease

A

not curative, but most will require surgery at some point.
e.g. temporary ileostomy, resection of part of bowel.
NOT bypass and pouch surgery, as too great a risk of recurrence to be worth doing.

72
Q

what areas of the GI tract may be affected by ulcerative colitis?

A

just rectum = proctitis.
extended to part of colon = left-sided colitis.
extended to entire colon = pancolitis.

73
Q

what is the impact of smoking on UC and Crohn’s, respectively?

A

UC - smoking is protective! incidence is higher in non-smokers.
Crohn’s - smoking doubles risk, and can precipitate relapses.

74
Q

describe the macro- and microscopic appearances of UC

A

macro - affects only colon, beginning in rectum and extending proximally. continuous involvement.
red mucosa, easy bleeding.

micro - mucosal inflammation (not full depth/transmural), no granulomata, goblet cell depletion, crypt abscesses.

75
Q

describe the symptoms of UC

A

episodic/chronic diarrhoea ± blood and mucus in stool.
crampy abdo discomfort.
bowel frequency relates to severity.
urgency/tenesmus => rectal UC.

76
Q

give 3 features of an acute, severe attack of UC

A

fever, malaise, anorexia, weight loss, tachycardia, tender distended abdomen

77
Q

give 3 extraintestinal signs of UC

A

clubbing, aphthous oral ulcers, erythema nodosum, episcleritis, conjunctivitis, iritis, large joint arthritis, ankylosing spondylitis, fatty liver, PSC, nutritional deficits, amyloidosis

78
Q

what investigations would you carry out in UC? what would they show?

A

colonoscopy - shows disease extent, allows biopsy for histo.

bloods - iron deficiency anaemia, low albumin, possible ANCA +ve.
stool MC&S to exclude infective causes.

79
Q

how would you treat UC?

A

mesalazine (a 5-ASA) + prednisolone.

20% will need surgery e.g. coleostomy with ilio-anal pouch.

80
Q

what are the 5Fs of abdominal distension?

A

Flatulence, Fat, Foetus, Fluid, Faeces

81
Q

list 3 causes of small/large bowel obstruction

A

small bowel - adhesions, hernias.

large bowel - colon carcinoma, constipation, diverticular stricture, volvulus.

82
Q

describe the clinical features you might see with a higher and lower intestinal obstruction

A

higher - vomiting, nausea, can still be passing bowel movements.
lower - no passage of faeces or flatulence

83
Q

what can be heard on examination in both large and small bowel obstruction?

A

tinkling bowel sounds

84
Q

how might you manage large/small bowel mechanical obstruction?

A

small may settle with conservative management - nasogastric suction, IV fluids.
large = surgery.

85
Q

give 3 causes of mechanical bowel obstruction

A

adhesions, hernias, Crohn’s disease, intussusception, obstruction due to extrinsic tumour, carcinoma of colon, sigmoid volvulus, diverticular disease

86
Q

how would mechanical bowel obstruction appear on abdo XR? and in functional obstruction?

A

mechanical - bowel is dilated above the level of obstruction.
functional - gas seen throughout bowel

87
Q

give 3 causes of functional bowel obstruction

A

paralytic ileus, pseudo-obstruction, post-surgery, peritonitis

88
Q

how would a functional bowel obstruction present differently from a mechanical obstruction?

A 
no pain (although peritonitis pain may be present if this is cause).
decreased bowel sounds.
89
Q

what is paralytic ileus?

A

adynamic bowel due to absence of normal peristaltic contractions

90
Q

give 3 possible causes of paralytic ileus

A

surgery, pancreatitis/peritonitis, spinal injury, hypokalaemia, hypnoatraemia, uraemia, peritoneal sepsis, tricyclic antidepressants

91
Q

what is pseudo-obstruction?

A

appears to be mechanical obstruction, but no cause is found

92
Q

which part of the bowel does mesenteric ischaemia involve and which vessel is occluded?

A

small bowel, superior mesenteric artery

93
Q

give 3 causes of mesenteric ischaemia

A

superior mesenteric artery thrombosis/embolism, non-occlusive disease, trauma, vasculitis, radiotherapy, strangulation

94
Q

how does mesenteric ischaemia present?

A

acute severe abdominal pain, no abdominal signs, rapid hypovolaemia leading to shock.

95
Q

describe the pain of mesenteric ischaemia

A

constant, central or around the RIF

96
Q

what is the main complication you would be worried about in a patient with mesenteric ischaemia?

A

septic peritonitis - possible progression of SIRS to multi-organ dysfunction syndrome

97
Q

what antibiotics would you give to a patient with mesenteric ischaemia?

A

gentamicin + metronidazole

98
Q

how would you treat mesenteric ischaemia?

A

fluid resus, abx, local thrombolysis (via catheter) or remove dead bowel surgically

99
Q

what vessel is blocked in ischaemic colitis?

A

inferior mesenteric artery

100
Q

how might a patient with ischaemic colitis present?

A

sudden onset abdominal pain and passing of bright red blood ± diarrhoea

101
Q

what characteristic feature would you see on abdo XR in a patient with ischaemic colitis?

A

‘thumb printing’ of splenic flexure

102
Q

what is the gold standard diagnostic investigation in ischaemic colitis?

A

colonoscopy + biopsy

103
Q

how would you treat ischaemic colitis?

A

fluid replacement + abx - most recover, left with strictures

104
Q

give 2 risk factors of ischaemic colitis

A

vasculitis, the Pill, thrombophilia, underlying CV disease

105
Q

name 2 secondary causes of pruritus ani

A

threadworm infestation, perianal eczema, fungal infection

106
Q

what are haemorrhoids?

A

disrupted and dilated anal cushions - there are 3 anal cushions, positioned where the 3 major arteries feeding the vascular plexuses enter the canal.

107
Q

in what location are haemorrhoids not painful and why?

A

internal/above the dentate line - lack of nerve supply, can only feel stretch.

108
Q

give 1 possible cause of haemorrhoids

A

constipation with prolonged straining.

congestion from pelvic tumour, pregnancy, CCF, portal hypertension

109
Q

what kind of bleeding would a patient with haemorrhoids experience?

A

bright red rectal bleeding - coating stools/on tissue/dripping into pan after defectaion

110
Q

give 2 possible features of haemorrhoids apart from bleeding?

what features would prompt you to consider other pathology?

A

haemorrhoids - mucous discharge, pruritus ani, severe anaemia.

other - weight loss, tenesmus, change in bowel habit

111
Q

give 2 differential diagnoses of haemorrhoids

A

perianal haematoma, anal fissure, abscess, tumour, proctalgia fugax

112
Q

what investigations should be performed on patients with suspected haemorrhoids?

A

abdo exam.
PR exam - prolapsing haemorrhoids are obvious, internal haemorrhoids aren’t palpable.
proctoscopy for internal haemorrhoids.
sigmoidoscopy.

113
Q

describe the management options for haemorrhoids

A

topical analgesics + stool softener.
rubber band ligation.
sclerosants - phenol injected into the pile.
infra-red coagulation.
surgical - excision haemorrhoidectomy, stapled haemorrhoidopexy.

114
Q

how do anal fistulae form?

A

track communicates between skin and anal canal/rectum.

deep intramuscular gland ducts are blocked - abscess form - discharge to form fistula.

115
Q

give 2 causes of anal fistulae

A

perianal sepsis, abscesses, Crohn’s disease, TB, diverticular disease, rectal carcinoma

116
Q

how would you treat an anal fistula?

A

fistulotomy + excision

117
Q

what are anal fissures?

A

painful tear in squamous lining of the lower anal canal

118
Q

give 2 causes of anal fissures

A

hard faeces.
parturition.

also - syphilis, herpes, trauma, Crohn’s, anal cancer, psoriasis

119
Q

how would you treat anal fissures?

A

local anaesthetic ointments (lidocaine/GTN) or topical diltiazem + stool softeners.

2nd line - botulinum toxin injection.

120
Q

where are perianal and pilonidal abscesses found in relation to the anus?

A

perianal - adjacent to anus.

pilonidal - 6cm above the anus.

121
Q

what is the cause of pilonidal abscesses?

A

obstruction of natal cleft hair follicles with ingrowing hair

122
Q

list some diseases that perianal abscess could be the first feature of

A

Crohn’s, UC, TB

123
Q

what are the 3 types of IBS?

A

IBS-C (constipation), IBS-D (diarrhoea), IBS-M (mixed).

124
Q

give 3 non-intestinal symptoms of IBS

A

painful periods, premenstrual tension, increased urination, nocturia, back pain, headaches, bad breath, poor sleeping, fatigue, anxiety, depression

125
Q

what are the diagnostic criteria for IBS?

A

abdo pain/discomfort must be relieved by defecation or associated with a change in stool form/bowel frequency.
AND 2 of:
urgency, incomplete evacuation, abdominal bloating distension, mucous PR, worsening of symptoms after food

126
Q

give 2 differential diagnoses of IBS

A

colonic cancer, IBD (crohn’s/UC), coeliac disease, gastroenteritis, diverticular disease.

127
Q

what is faecal calprotectin, and when would you test for it?

A

a marker of bowel inflammation - test for it in diarrhoea, to differentiate between IBD and IBS - faecal calprotecin will be raised in IBD as it is an inflammatory disease.

128
Q

what investigations should a patient with suspected IBS be given and what would they show?

A

FBC, ESR, CRP, faecal calprotectin and coeliac antibody screen (for EMA and TTG).

129
Q

how would you manage IBS?

A

diet - avoid fibre, fructose, wheat, starch, caffeine, alcohol etc.

constipation = biscodyl and sodium picosulphate (laxatives).

diarrhoea - bulking agent ± loperamide after each loose stool.

colic/bloating - antispasmodics - mebervine, simeticone etc

130
Q

what is a diverticulum? define diverticulosis and diverticulitis.

A 
diverticulum = outpouching of the gut wall.
diverticulosis = presence of diverticula.
diverticulitis = inflammation of diverticula (usually when faeces obstruct the neck of the diverticulum)
131
Q

what causes diverticula to form?

A

thickened muscle layer and high intraluminal pressure (constipation) which forces pouches of mucosa to herniate through the muscular wall at weak points

132
Q

how are diverticula generally diagnosed?

A

usually asymptomatic, so commonly an incidental finding at colonoscopy.

133
Q

what is the best investigation to confirm acute diverticulitis?

A

CT

134
Q

how would diverticulitis present?

A

L iliac fossa pain, fever, nausea, raised WCC, raised CRP/ESR.
tender colon ± localised/generalised peritonitis.

135
Q

name 2 possible complications of diverticulitis

A

perforation, abscess formation, peritonitis, formation of fistulas into bladder/vagina, intestinal obstruction.

136
Q

how would you treat diverticulitis?

A

analgesia, nil by mouth, IV fluid, abx, CT-guided percutaneous drainage if abscess develops.

137
Q

name 2 things that may obstruct the lumen of the appendix, allowing gut organisms to invade the appendix wall and leading to appendicitis?

A

lymphoid hyperplasia, faecolith, filarial worms.

138
Q

what is the classical feature of appendicitis?

A

periumbilical pain that moves to right iliac fossa

139
Q

give 3 signs of appendicitis

A

tachycardia, fever, furred tongue, lying still, coughing hurts, shallow breaths, guarding of RIF, rebound + percussion tenderness in RIF.

140
Q

what are the 3 painful signs you would examine for in appendicitis?

A

Rovsing’s sign - pain greater in RIF than LIF when LIF pressed.
Psoas sign - pain on extending hip.
Cope sign - pain on flexion and internal rotation of right hip.

141
Q

what are 3 differential diagnoses of appendicitis?

A

Gynae problems - ruptured ectopic etc - do pregnancy test!
Inflamed Meckel’s diverticulum.
functional bowel disease (IBD, IBS)

142
Q

describe the management of appendicitis

A

metronidazole and cefuroxime.

prompt appendicectomy.

143
Q

what patient groups are at greater risk of primary peritonitis?

A

liver disease - spontaneous bacterial peritonitis (SBP).

females, immunocompromised, peritoneal dialysis, ascites.

144
Q

give 3 examples of causes of secondary peritonitis

A

perforation of hollow viscus, inflammation of abdo organs, peritoneal dialysis, TB, ischaemia of a hollow viscus, chemical.

145
Q

give 3 symptoms of peritonitis

A

pain, tendenderness, nausea, chills, rigor, dizziness, weakness and inability to move due to pain

146
Q

give 3 signs you might find on examination of a peritonitis patient

A

pyrexia, tachycardia, confusion, guarding, rebound, rigidity, silent abdomen, patient lies very still

147
Q

what investigations would you perform on a patient with peritonitis?

A

CXR - look for free air under the diaphragm.

US/CT

148
Q

how would you manage peritonitis?

A

ABCs, abx, surgical repair of perforated viscus.

149
Q

what is volvulus?

A

bowel obstruction due to a loop of bowel that has twisted around the site of its mesenteric attachment

150
Q

what might be seen on abdominal X ray in a patient with sigmoid volvulus?

A

‘inverted U’ loop - coffee bean

151
Q

how would you treat a sigmoid volvulus?

A

sigmoidoscopy, insertion of a flatus tube.

152
Q

what might be found on examination of a patient with sigmoid volvulus?

A

distension of abdomen, increased ‘tinkling’ bowel sounds, tenderness (suggests ischaemia).

153
Q

describe what occurs in a sliding hiatus hernia

A

gastro-oesophageal junction slides up into the chest.

acid reflux common - LOS is less competent.

154
Q

describe what occurs in a rolling hiatus hernia

A

gastro-oesophageal junction remains in the abdomen, but a bulge of stomach herniates up into the chest alongside the oesophagus - can strangulate.

acid reflux uncommon - LOS is intact.

155
Q

how would you investigate a hiatus hernia?

A

barium swallow.

upper GI endoscopy.

156
Q

how might you manage a hiatus hernia?

A

weight loss, treat reflux symptoms.

surgery - if intractable symptoms, or a rolling hernia - Nissen fundoplication

157
Q

give 2 conditions that predispose to inguinal hernias

A

male sex, chronic cough, constipation, urinary obstruction, heavy lifting, ascites, past abdominal surgery

158
Q

in relation to pubic tubercle, where does an inguinal hernia present?

A

superior and medial

159
Q

what is the difference between a direct and indirect inguinal hernia?

A

indirect - passes through inguinal canal into testicle due to failure in embryonic closure.
direct - enters through weak point in the transversalis fascia (the posterior wall of the inguinal canal) - Hesselbach’s triangle.

160
Q

where might a lump from a femoral hernia present in a patient?

A

inner upper thigh, pointing down the thigh

161
Q

where, in relation to the pubic tubercle, is a femoral hernia felt?

A

inferior and lateral

162
Q

give 3 causes of an incisional hernia

A

infection, increased abdo pressure, poor surgical technique, obesity, haematoma

163
Q

what are the 3 types of liver abscess?

A

pyogenic, amoebic or hyatid

164
Q

give 3 causes of pyogenic liver abscess

A

*idiopathic.
biliary sepsis
portal pyaemia from intra-abdominal sepsis
trauma
bacteraemia
direct extension from e.g. perinephric abscess

165
Q

list the most common causative organisms in liver abscesses

A

E coli, Strep milleri.

anaerobes e.g. bacterioides

166
Q

what causes an amoebic liver abscess?

A

spread of entamoeba histolytica from bowel to liver via portal system

167
Q

what is the main GI feature of amoebic liver abscess?

A

bloody diarrhoea

168
Q

what would you see on performing blood investigations on a patient with a pyogenic liver abscess?

A

raised serum bilirubin, normocytic anaemia, raised alkaline phosphatase, ESR, serum B12

169
Q

if you took a stool culture and liver aspiration of an amoebic abscess patient, what would you see?

A

faeces - pus and amoeba trophozoites.

liver aspiration - ‘anchovy sauce’ pus

170
Q

how would you manage an amoebic liver abscess?

A

metronidazole. no need to aspirate.

171
Q

how would you manage a pyogenic abscess?

A

percutaneous aspiration under radiological (e.g. US) control.
pig tail catheter for continuous drainage.
IV metronidazole and cefuroxime.

GI (5 decks)

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