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Year 3 Conditions - Jan > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

Define GORD

A

Inflammation of the oesophagus caused by reflux of gastric acid and/or bile

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2
Q

Aetiology of GORD

A

Disruption of mechanism preventing reflux
Prolonged oesophageal acid clearance
increased dietary fat

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3
Q

Heartburn - aggravated by lying supine, bending, large/fatty meals
Antacids pain relief
Waterbrash
Dysphagia

A

Symtoms & signs of GORD

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4
Q

Investigations for GORD

A

PPI tria

OGD

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5
Q

Management for GORD

A

Advice - weight loss, lower fat meals
Medical - PPI, antacids,
Surgery - antireflux surgery

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6
Q

Complications of GORD

A
  • Oesophageal ulceration
  • Haemorrhage
  • Oesophageal stricture
  • Barrett’s oesophagus
  • Oesophageal adenocarcinoma
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7
Q

Define Barrett’s oesophagus

A

Metaplastic change: simple –> columnar

Can progress to oesophageal adenocarcinoma

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8
Q

Aetiology Barrett’s oesophagus

A

GORD

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9
Q

Heartburn
Dyspnoea
Can be asymtpomatic

A

Barrett’s oesophagus - Symptoms & Signs

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10
Q

Investigations for Barrett’s

A

OGD & Biopsy

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11
Q

Management plan for Barrett’s

A 
•	Non-dysplastic 
PPI (omeprazole)
Surveillance 
2nd line: Anti-reflux surgery 
•	Low grade dysplasia (nodule only)
Radiofrequency ablation +/- endoscopic mucosal resection 
•	High grade dysplasia 
Radiofrequency ablation 
PPI 
2nd line: Oesophagostomy
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12
Q

Complications of Barrett’s

A

Oesophageal adenocarcinoma development

Risk of dysplasia

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13
Q

Define hiatus hernia

A

• Protrusion of intra-abdominal contents through an enlarged oesophageal hiatus of the diaphragm

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14
Q

Aetiology hiatus hernia

A

Congenital
Traumatic

Non – Traumatic
o Sliding (80%) – hernia moves in & out of chest –> Acid reflux often happens as LOS becomes less competent
o Paraoesophageal (rolling - 20%) – hernia goes through hole in diaphragm next to oesophagus
o Gastro-oesophageal junction intact acid reflux uncommon
o Mixed

Risk factors 
o	Obesity 
o	Low-fibre diet 
o	Chronic oesophagitis 
o	Ascites 
o	Pregnancy
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15
Q

• Most are Asymptomatic
• GORD Sx & painless regurgitation = hiatus hernia
o Heartburn
o Waterbrash
o Dull retrosternal chest pain (often associated with swallowing)
Maybe bowel sounds in chest

A

Hiatus hernia

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16
Q

Investigations for hiatus hernia

A

CXR –> retrocardia gastric air bubble

Endoscopy –> detects oesophagitis but can rule out hiatus hernia

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17
Q

Management plan for hiatus hernia

A

Medical
- o Modify lifestyle factors (eg. lose weight etc)
o Inhibit acid production (PPI)
o Enhance upper GI motility

Surgical
o Nissen fundoplication
♣ Stomach pulled down through oesophageal hiatus and part of stomach wrapped (360) around oesophagus to make new sphincter and ↓ likelihood of herniation
o Belsey Mark IV Fundoplication
♣ 270 wrap
o Hill repair
♣ Gastric cardia is anchored to posterior abdominal wall

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18
Q

Complications of hiatus hernia

A 
Oesophageal 
o	Intermittent bleeding 
o	Oesophagitis 
o	Erosions 
o	Barrett's oesophagus 
o	Oesophageal strictures

Non-Oesophageal
o Incarceration of hiatus hernia (only with paraoesophageal hernias)
o This can lead to strangulation and perforation

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19
Q

Define Mallory-Weiss tear

A

• Tear or laceration of the lining of the oesophagus around the junction with the stomach, because of violent vomiting or straining to vomit

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20
Q

Aetiology of Mallory-Weiss tear

A

• Caused by prolonged violent vomiting (or anything else that causes ↑ in pressure)

Risk factors
o	Chronic cough 
o	Hiatal hernia 
o	Significant alcohol use 
o	Bulimia 
o	Trauma (ie. Previous instrumentation, retching during endoscopy)
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21
Q
  • Most cases don’t have any Sx
  • Abdominal pain
  • Severe vomiting
  • HAEMATEMESIS –> Can be from flecks to bright red bloody vomit
  • Light-headedness/dizziness
  • Postural hypotension
  • Malena
A

Mallory Weiss tear

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22
Q

Investigations for Mallory Weiss tear

A

FBC
CXR
OGD

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23
Q

Management plan for Mallory Weiss tear

A

1st line
Monitoring
Endoscopy +/- Antigastric acid therapy, antiemetic, somatostatin analogue

2nd Line
Surgery

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24
Q

Complications of Mallory Weiss tear

A

Re-bleeding
MI
Oesophageal perforation

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25
Q

Define peptic ulcer

A

• Break in the mucosal lining of the stomach or duodenum > 5mm in diameter, with depth to the submucosa.

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26
Q

Aetiology of peptic ulcer disease

A

• Results from an imbalance between factors promoting mucosal damage (gastric acid, pepsin, H. pylori infection, NSAIDs) and mechanisms promoting gastroduodenal defense (prostaglandins, mucus, bicarbonate, mucosal blood flow)
• Risk factors:
o H. pylori infection
o NSAID use
o Smoking
o Age
o RARE: Zollinger-Ellison syndrome syndrome of gastric acid hypersecretion caused by gastrin secretion neuro-endocrine tumour
• NOTE: Duodenal ulcers are almost always associated with H. pylori infection and gastric ulcers with NSAID use

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27
Q
  • Abdominal pain or discomfort centred in the upper abdomen
  • Relieved by antacids

Variable relationship to food intake:
Gastric – pain is worse soon after eating
Duodenal – pain is worse several hours after eating

• Some epigastric tenderness

A

Peptic ulcer disease

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28
Q

Investigations for Peptic ulcer disease

A 
•	If <55 and no red flags 
o	H pylori breath test/stoll antigen test 
o	FBC
o	Stool occult blood test
o	Serum gastrin

• If >55 or red flags or treatment fails
o Upper GI endoscopy & biopsy
o If ulcer present: repeat endoscopy 6-8 weeks after treatment to confirm resolution and exclude malignancy

•	H. pylori 
o	Urea breath test:
♣	Radio-labelled urea given by mouth
♣	C13 detected in expelled air 
o	Stool antigen test

• Upper Gastrointestinal endoscopy
o Biopsies of gastric ulcers to rule out malignancy
o Dueodenal ulcers don’t need to be biopsied

•	FBC
o	FBC (for anaemia)
o	Serum amylase (to exclude pancreatitis)
o	U&amp;Es
o	Clotting screen
o	LFT
o	Cross-matching if active bleeding 
o	Secretin test (if Zollinger-Ellison syndrome suspected) – IV secretin causes a rise in serum gastrin in ZE patients but not in normal patients
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29
Q

Management plan for Peptic ulcer disease

A

• Acute (active bleeding ulcer)
o Endoscopy +/- blood transfusion
o Proton pump inhibitor omeprazole
o Surgery only if ulcer has perforated or bleeding can’t be controlled with endoscopy

•	If H. pylori is present:
o	Triple therapy (14 days)  PPI plus 2 antibiotics
♣	Omeprazole 20 mg bd
♣	Clarithromycin 500mg bd 
♣	Amoxicillin 1000mg bd
  • Can also use a H2 antagonist to supress acids ranitidine 150 mg BD
  • Misoprostol (PGI E1 analogue) can be used if NSAIDs can’t be stopped
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30
Q

Complications of Peptic ulcer disease

A
  • Penetration into a surrounding organ (ie pancreas)
  • Gastric outlet obstruction
  • Upper GI bleeding
  • Perforation
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31
Q

Define GI perforation

A

• Perforation of the wall of the GI tract with spillage of bowel contents

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32
Q

Aetiology of GI perf

A 
Large bowel (common)  remember CAD UV
o	Colorectal cancer 
o	Diverticulitis 
o	Appendicitis 
o	Others: volvulus, ulcerative colitis (toxic megacolon)

Gastroduodenal
o Common perforated duodenal or gastric ulcer
o Others: gastric cancer

Small bowel (rare)
o Trauma
o Infection (eg. TB)
o Crohn’s disease

Oesophagus
o Boerhaave’s perforation – rupture of the oesophagus following forceful vomiting

Risk factors
o	Cause (eg. gastroduodenal – NSAIDs, steroids, bisphosphonates)
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33
Q

• Large Bowel
o Peritonitic abdominal pain
o IMPORTANT: make sure you rule out ruptured AAA
• Gastroduodenal
o Sudden-onset severe epigastric pain - worse on movement
o Pain becomes generalised
o Gastric malignancy - may have accompanying weight loss and nausea/vomiting
• Oesophageal
o Severe pain following an episode of violent vomiting
o Neck/chest pain and dysphagia develop soon afterwards

Signs of Shock 
Pyrexia 
pallor 
Dehydraiton 
Signs of peritonitis 
Loss of liver dullness (due to overlying gas)
A

GI perforation

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34
Q

Investigations for GI perforation

A

Blood
o FBC, U&E – urea raised after upper GI bleed, LFTs
o Amylase - will be raised with perforation (but should not be astronomical (as seen in pancreatitis))

Erect CXR
o Shows air under the diaphragm

AXR
o Shows abnormal gas shadowing

Gastrograffin Swallow
o For suspected oesophageal perforations

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35
Q

Management plan for GI perforation

A

Resuscitation
o Correct fluid and electrolytes
o IV antibiotics (+ anaerobic cover) – cefuroxime and metronidazole

Surgical
o	Large Bowel
•	Identify site of perforation 
•	Peritoneal lavage 
•	Resection of perforated section (usually as part of a Hartmann's procedure)

o Gastroduodenal
• Laparotomy
• Peritoneal lavage
• Perforation is closed with an omental patch
• Gastric ulcers are biopsied – malignancy
• Helicobacter pylori eradication if positive for H. pylori

o Oesophageal
• Pleural lavage
• Repair of ruptured oesophagus

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36
Q

Complications of GI perforation

A
  • Large and Small Bowel - peritonitis

* Oesophagus - mediastinitis, shock, overwhelming sepsis and death

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37
Q

Define gastric cancer

A 
•	Neoplasm that can develop in any portion of the stomach and mayb spread to lymph nodes and other organs
•	Most commonly adenocarcnioms 
o	Rarer causes:
♣	Lymphoma
♣	Leiomyoscarcoma
38
Q

Aetiology of Gastric cancer

A 
Risk factors:
o	Pernicious anaemia 
o	H. pylori infection 
o	N-nitroso compounds 
o	Weak:
♣	Diet low in fruits and vegetables 
♣	High-salt diet 
♣	Smoking 
♣	FHx
39
Q

Early satiety
Epigastric discomfort
Weight loss
Maybe malaena

Abdominal tenderness
Abdominal mass
Virchow's node
Sister Mary Joseph's nodule
Irish node
A

Gastric cancer

40
Q

Investigations for gastric cancer

A
  • Upper GI endoscopy with biopsy
  • Endoscopic USS determines clinical tumour and node stage
  • CT/MRI to check for spread
  • Laparoscopy maybe needed to determine if tumour resectable
41
Q

Define anal fissure

A
  • A painful tear in the squamous lining of the lower anal canal
  • 90% of the fissures are posterior (anterior only tend to happen after childbirth)
42
Q

Aetiology of anal fissure

A
  • assing hard stool bolus

* Spasm of the anal sphincter can constrict inferior rectal artery, causing ischaemia and impairing healing process

43
Q

Tearing pain upon defecation
Blood seen upon wiping
Tear in squamous lining of anus upon examination

A

Anal fissure

44
Q

Investigation for anal fissure

A

Inspection of anus

45
Q

Management of anal fissure

A

• Conservative
o High-fibre diet
o Adequate fluid intake
o Stool softeners

  • Topical glyceryl trinitrate relaxes anal sphincter and promotes healing
  • Topical diltiazem if GTN is intolerable
46
Q

Complications of anal fissure

A

Chronic anal fissure

47
Q

Define rectal prolapse

A

• Abnormal protrusion of the full thickness (or only mucosal layer) of rectum through the anus

48
Q

Aetiology of rectal prolapse

A
  • Straining
  • Abnormal rectal anatomy or physiology (eg. pelvic floor weakness, poor fixation of rectum to sacrum or ↓ anal sphincter pressure)
•	Risk factors
o	Constipation 
o	Causes of ↑ straining 
o	Cystic fibrosis (in children)
o	Previous trauma to anus/perineum 
o	Neurological conditions (e.g. cauda equina syndrome, MS)
49
Q
  • Protruding anal mass
  • Initially associated with defecation
  • May require digital replacement
  • Constipation
  • Faecal incontinence – in 75%
  • PR mucus or bleeding
  • May be an Emergency – irreducible or strangulated prolapse
A

Rectal Prolapse

50
Q

Investigations for rectal prolapse

A

• Imaging
o Proctosigmoidoscopy
o Defecating proctogram or barium enema

• Other
o Anal sphincter manometry
o Pudendal nerve studies

• Sweat Chloride Test
o Performed in children to test for cystic fibrosis

51
Q

Define colorectal cancer

A
  • Malignant adenocarcinoma of the large bowel
  • 71% arise in colon
  • 21% rectum
52
Q

Aetiology of colorectal cancer

A

• Sequence of genetic changes going from normal bowel epithelium to cancer
o APC COX2 over expression K-Ras p53)
o Sequence from epithelial dysplasia to adenoma to carcinoma
• Risk factors
o Western diet (e.g. red meat, alcohol, low fibre)
o Smoking
o Colorectal polyps
o Previous colorectal cancer
o FHx
o IBD
o Chronic bowel inflammation eg. IBD

53
Q 
Change in bowel habit
Rectal bleeding 
Anaemia 
Weight loss
Non-specific malaise
Abdo mass
A

Colorectal carcinoma

54
Q

Investigations for Colorectal carcinoma

A

• Bloods
o FBC – anaemia
o LFTs
o Tumour markers (CEA)

• Endoscopy
o Colonoscopy
♣ Can be used to biopsy the tumour

• Double-contrast Barium Enema
o May show ‘apple core’ strictures

• Abdominal ultrasound for hepatic metastases

• Contrast CT
o For staging (Duke’s staging)

55
Q

Define hepatocellular carcinoma

A

• Primary malignancy of liver parenchyma

56
Q

Aetiology hepatocellular carcinoma

A 
o	Chronic liver damage
♣	Alcoholic liver disease
♣	Hepatitis B
♣	Hepatitis C
♣	Autoimmune disease

o Metabolic disease
♣ Haemochromatosis

o Aflatoxins
♣ Aspergillus flavus – cereals contaminated with fungi

57
Q 
RUQ pain
Malaise
Weight loss 
Loss of appetite 
Abdo distension
Jaundice 
Spider naevi 
Palmar erythema
Ascites 
Hepatosplenomegaly 
Asterixis 
Cachexia 
Fetor hepaticus
A

Hepatocellular carcinoma

58
Q

Investigations Hepatocellular carcinoma

A

• Bloods
o FBC
o U&Es
♣ Hyponatraemia fluid overload
♣ High urea 2o to renal problems
o LFTs
♣ ↑ Transaminases, ALP & bilirubin Chronic liver disease & Cirrhosis
♣ ↓ albumin Chronic liver disease & cirrhosis
o Viral hepatitis panel to determine cause
o a-fetoprotein - ↑

• Imaging
o Abdominal US – poorly defined margins and coarse, irregular internal echoes
o CT/MRI Abdo – for staging

• Histology/Cytology
o Liver biopsy
o Ascitic tap

59
Q

Define Volvulus

A

• Rotation of a loop of bowel around the axis of its mesentery that results in bowel obstruction and potential ischaemia
• Areas usually affected:
o Sigmoid colon – 65%
o Caecum – 30%
o Volvulus Neonatorum – occurs in neonates and typically affects midgut

60
Q

Aetiology of Volvulus

A
  • Anatomical factors (e.g. long mesentery)
  • Risk factors
o	Adults 
♣	Long sigmoid colon 
♣	Long mesentery
♣	Mobile caecum 
♣	Chronic constipation 
♣	Adhesions 
♣	Chagas disease
♣	Parasitic infections

o Neonatal
♣ Malrotation

61
Q
  • Severe colicky abdominal pain and swelling
  • Absolute constipation
  • Vomiting
Abdominal distension &amp; tenderness
Absent or tinkling bowel sounds 
Fever 
Tachycardia
Dehydraiton signs
A

Volvulus

62
Q

Investigations for volvulus

A 
•	AXR
•	Erect CXR – if perforation is suspected 
•	Water soluble contrast enema
o	Shows site of obstruction 
CT Scan
63
Q

Define Liver abscesses and cyst

A
  • Abscess: liver infection resulting in a walled of collection of pus
  • Cyst: liver infection resulting in a walled off collection of cyst fluid
64
Q

Aetiology of liver abscess and cyst

A 
•	Pyogenic (producing pus)
o	E. coli
o	Klebsiella 
o	Enterococcus
o	Bacteriodes
o	Streptococci
o	Staphylococci
o	60% caused by biliary tract disease (e.g. gallstones, strictures, congenital cysts)
o	15% have unknown cause
  • Amoebic abscess caused by Entamoeba histolytica
  • Hydatid cyst caused by tapeworm Echinococcus granulosis
  • TB
65
Q
  • Fever
  • Malaise
  • Nausea
  • Anorexia
  • Night sweats
  • Weight loss
  • RUQ/epigastric pain which maybe refered to shoulder
  • Jaundice
  • Diarrhoea
  • Pyrexia of unknown origin
  • Ask about foreign travel
  • Fever – continuous or spiking
  • Jaundice
  • Tender hepatomegaly (right lobe affected more than left)
  • Right lung base dullness to percussion and ↓ breath sounds caused by reactive pleural effusion
A

Liver abscess and cyst

66
Q

Investigations for liver abscess and cyst

A 
•	Bloods
o	FBC
♣	Mild anaemia 
♣	Leukocytosis 
♣	↑ eosinophils in hydatid disease
o	LFTs
♣	↑ ALP
♣	↑ bilirubin 
o	↑ ESR and CRP
o	Blood cultures
o	Ameobic and hydatid serology
  • Stool MC&S for E. histolytica or tapeworm eggs
  • Liver US or CT/MRI localised structure of mass
  • CXR check for right pleural effusion or atelectasis, raised diaphragm

• Aspiration and cluture of abscess material:
o Most pyogenic liver abscesses are polymicrobial
Amoebic abscesses have fluid of necrotic hepatocytes and trophozites

67
Q

Define NASH

A

• A term used to describe a range of conditions caused by the build-up of fat in the liver due to causes other than excessive alcohol use.

68
Q

Aetiology of NASH

A

• Liver may become initially fatty due to alcohol abuse. Yet these tend to resolve within days.
• If fat persists, can cause inflammation and fibrosis (steatohepatitis) NASH is this without Hx of alcoholism.
• Aetiology process is multifactorial
o First hit of imbalance of fatty acid metabolism which leads to hepatic triglyceride accumulation
o Second hit of dysregulated cytokine production due to efforts to compensate for altered lipid homeostasis

•	Risk factors
o	Obesity 
o	T2DM
o	HTN
o	Hypercholeesterolaemia 
o	Age > 50 yrs 
o	Smoking
o	Total Parenteral Nutrition
69
Q 
•	Often no symptoms or very vague in early stages  found as incidental findings 
•	Occasional Sx include:
o	Dull or aching RUQ pain 
o	Fatigue 
o	Unexplained weight loss 
o	Weakness

RUQ pain/tenderness

A

NASH

70
Q

Investigations for NASH

A 
•	LFTs
o	Elevated AST and ALT
o	Elevated bilirubin
o	Elevated ALP
o	Elevated GGT

• Fasting lipid panel
o Elevated total cholesterol, LDL, triglyceride
o Low HDL

• Liver biopsy

71
Q

Management plan for NASH

A 
•	Conservative – controlling risk factors:
o	Blood pressure
o	Diabetes
o	Cholesterol 
o	Weight loss
o	Stop smoking 
o	Exercise regularly 
o	↓ alcohol consumption (drinking can make it worse)
72
Q

Complications of NASH

A

Cirrhosis –>

o	Ascites 
o	Oesophageal varices 
o	Hepatic encephalopathy 
o	Hepatocellular carcinoma 
o	End-stage liver failure
73
Q

Define haemochromatosis

A
  • Autosomal recessive disease in which ↑ intestinal absorption of iron causes accumulation of iron in tissues which may lead to organ damage.
  • You get iron deposition in joints, liver, heart, pancreas, pituitary, adrenals and skin
74
Q

Aetiology haemochromatosis

A

• Mutation of the HFE gene, found on CHr6.
• A model for pathogenesis suggested;
o Liver model – HFE deficiency = ↓ hepatic hormone ‘hepcidin’ ↑ intestinal iron absorption (lack of inhibitory effect of hepcidin on ferroportin protein which exports iron from enterocytes into circulation)

75
Q 
o	Fatigue
o	Weakness 
o	Arthropathy 
o	Erectile dysfunction 
o	Heart problems 
o	Small/large joint pains 
o	Hepatomegaly
o	Diabetes mellitus 
o	Hypogonadism  impotence and loss of libido
o	Cardiac failure  arrhythmias and HF
A

Haemochromatosis

76
Q

Investigations for haemochromatosis

A

• Haematinics
o Serum Ferritin HIGH (NOTE: not v accurate because is acute phase protein)
o Serum Transferrin Low
o Serum transferrin saturation High

• Tests to exclude other causes of high ferritin
o CRP – inflammation
o Chronic alcohol consumption
o ALT – liver necrosis

  • Liver MRI – for Fe overload
  • Liver Biopsy – iron content would be raised
  • ECG/ECHO if cardiomyopathy suspected
77
Q

Define PBC

A
  • Chronic disease of small intrahepatic bile ducts characterised by progressive bile duct damage occurring in the context of chronic portal tract inflammation.
  • Fibrosis develops as a consequence, and secondary effects of toxic bile retained in liver results ultimately in cirrhosis
78
Q

Aetiology PBC

A

• Thought to be autoimmune
o Link to high personal and family incidence of other AI processes
• Genetic and environment facts also involved
• Environmental trigger may cause bile duct epithelial injury, which then leads to T-cell mediated AI response directed against bile duct epithelial cells

79
Q

• Often incidental in finding on blood tests
• Insidious onset with vague Sx such as:
o Fatigue
o Weight loss
o Pruritus
• Rarely, may cause discomfort in RUQ
• May present with complication of liver decompensation (e.g jaundice, ascites, variceal haemorrhage)
• May present with Sx of associated conditions (e.g Siogren’s syndrome, arthritis, Raynaud’s phenomenon)

•	Early – maybe no signs 
•	Late
o	Jaundice 
o	Skin pigmentation 
o	Scratch marks 
o	Xanthomas (2O to hypercholesterolaemia)
o	Hepatosplenomegaly 
o	Ascites 
o	Signs of chronic liver disease
A

PBC

80
Q

Investigations for PBC

A 
•	Bloods 
o	LFTs
♣	↑ ALP
♣	↑ GGT
♣	Elevated bilirubin 
♣	Transaminases int normally, but ↑ with disease progression 
♣	Low albumin

• Typical features of PBC
o Antimitochondrial antibody – hallmarks of PBC
o High IgM
o High cholesterol

  • TFTs – PBC associated with AI thyroid disease
  • USS – exclude extrahpepatic biliary obstruction (eg. gallstones)

• Liver biopsy
o Chronic inflammatory cells and granulomas around intrahpepatic bile ducts, destruction of bile ducts, fibrosis and regenerating nodules of hepatocytes

81
Q

Appendicitis Aetiology

A

• Obstruction of the lumen of appendix is main cause of acute appendicitis by:
o Faecolith (hard mass of faecal matter)
o Normal stool
o Lymphoid hyperplasia
• Can lead to oedema, ischaemic necrosis and perforation

82
Q 
Periumbilical pain moving to RIF
Anorexia
Vomiting 
Constipation 
Diarrhoea
A

Sx of Appendicitis

83
Q 
•	General signs 
o	Tachycardia
o	Fever
o	Furred tongue 
o	Lying still 
o	Coughing hurts
o	Foetor with/without flushing 
o	Shallow breaths 
•	RIF signs 
o	Guarding 
o	Rebound and percussion tenderness

o Rovsing’s Sign – palpation of LIF causes more pain in RIF than left
o Psoas Sign – pain on extending hip (caused by retrocaecal appendix)
o Obturator Sign – pain on flexion and internal rotation of the hip (occurs if appendix is in close proximity to obturator internus)

A

Signs of Appendicitis

84
Q

Investigations for Appenditicits

A

• FBC
o ↑ WCC
o ↑ CRP
o Pregnancy test – to rule out ectopic pregnancy
• Abdo & Pelvis CT scan
o High diagnostic accuracy but may cause fatal delay – usually go straight to surgery for diagnostic laparoscopy +/- appendicectomy
• Abdominal USS

85
Q

Mamangement - appendicits

A
  • Prompt appendicectomy (could be done laparoscopically)
  • Antibiotics Cefoxitin
  • IV fluids should be started
86
Q

Complications of appendicits

A
  • Perforation
  • Appendicular mass when inflamed appendix is covered with omentum
  • Generalised peritonitis
  • Appendix abscess if mass fails to resolve, treatment involves drainage and Abs
87
Q

Define pilonidal sinus

A

Forceful insertion of hairs into skin of natal cleft in sacrococcygeal area promotes chronic inflammatory reaction, causing epithelialized sinus.

88
Q

Aetiology pilonidal sinus

A
  • Ingrowing of hairs excited foreign body inflammatory reaction and may cause 2O tracks to open laterally +/- abscesses with foul-smelling discharge
  • Intermittent negative pressure will draw in more hair and perpetuate the cycle

• Risk factors:
o Hirsutism
o Spending long time sitting down
o Occupational (eg. hairdressers may develop interdigital pilonidal sinus)

89
Q
  • Painful natal cleft
  • Discharging swelling & foul smell
  • Often recurrent
  • Deep skin of natal cleft often macerated, with one or several sinuses opening into or just lateral to midline
  • Hairs may protrude from the swelling
  • If infection or abscess, the swelling will become tender
  • It may be fluctuant and discharge pus or blood-stained fluid on compression
A

Pilonidal sinus

90
Q

Investigations for pilonidal sinus

A

• NONE needed
• Bloods - to check for signs of infection
o Raised WCC
o Fasting glucose (diabetics are at risk)

91
Q

Management for pilonidal sinus

A

• Consider pre-op Abs

• Acute Pilonidal Abscess
o Incision and drainage

• Chronic Pilonidal Sinus
o Excision under general anaesthesia with exploration

• Prevention
o Good hygiene
o Shaving

92
Q

Complications pilonidal sinus

A
  • Pain
  • Infection
  • Abscess
  • Recurrence

Year 3 Conditions - Jan (9 decks)

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