GI Flashcards
SBO causes
COMMON
- Adhesions (postoperative) 50–80%
- Hernias (external) 5–15%
- Malignancy (peritoneal) 5–15%
- Crohn’s disease <7%
OTHER
- Bowel wall lesions (causing intussusception)
- Intra-luminal mass: foreign body, gallstone ileus
- Extrinsic inflammatory lesions (appendiceal)
- Internal hernia
- Congenital malformation
- Superior Mesenteric Artery syndrom
Large Bowel Obstruction
Tumor (usually sigmoid carcinoma)
Volvulus (sigmoid, cecal)
Fecal impaction
Diverticulitis
Benign stricture (e.g. post-operative, inflammatory bowel disease)
Abscess
BO vs Ileus
Dysentry
Bacterial
- Gram positive – Clostridium Difficile
- Gram negative – Shigellosis, Enterohaemorrhagic E.coli, Salmonella, Yersinia enterocolitica
Protozoa
- Entamoeba histolytica
- Balantidium coli
Helminths
- Schistoma (S. mansion or S. japonicum)
- Ascariasis
- Trichuriasis
Non-infectious
- Inflammatory bowel disease
- Colorectal cancer
- Polyps
- Ischaemic colitis
Mackler’s Triad (oesophageal rupture)
- Chest pain
- Vomiting
- SC emphysema
Pathognomic for spontaneous oesophageal rupture - < 50% presentations
CXR oesophageal rupture
Abnormalities in up to 90% (none if early)
Pneumomediastinum
Right pl effusion - upper third rupture
Left pl effusion with distal third rupture
SC emphysema
Mediastinal widening
Pulmonary infiltrates
Oesophageal narrowings (4)
- C6 - cricopharyngeus muscle
- T4 - aortic arch
- T6 - bifurcation of trachea
- T11 - gastrooesophageal junction
Dysphagia - Neuromuscular
VASCULAR
- CVA
IMMUNOLOGICAL
- Dermatomyositis
- MS
- Myaesthenia gravis
- Polio
- Scleorderma
INFECTIOUS
- Botulism
- Diptheria
- Polio
- Rabies
- Sydenham’s chorea
- Tetanus
METABOLIC
- Lead poisoning
- Mg deficiency
OTHER
- Alzheinmer’s
- Amyotrophic lateral sclerosis
- Brain tunmour
- Depression
- Diabetic neuropathy
Dysphagia - Obstructive
- Aortic aneurysm
- Oesophageal dysmotility
- Oesophageal - rings, webs, stricture
- Oesophagitis
- FB
- Hypertrophic cervical spurs
- Mediastinal mass
- Left atrial enlargement
- Thyroid enlgargment
- Vascular anomalies
*
Dysphagia - other
- Alcoholism
- Decreased saliva production - Sjogren’s, radiation SE
- DM
- GORD
- Post-op
- Functional
Internal Hernia Locations
Haemorrhoid grades
- Painless, no prolapse
- Prolapse afters straining, spontaneous reduction
- Prolapse, require digital reduction
- Prolapse, irreducible
GI bleeding Risk Factors
- Medications
- Antiplatelets
- Anticoagulants
- NSAIDS
- Steroids
- PMHx
- PUD
- Chronix liver Dx
- Cirrosis
- Age >60yrs
- ETOH
- Smoker
- Comorbidities
- CCF
- DM
- Renal failure
- Malignancy
- AAA graft
UGI Bleed Mimics
- Epistaxis
- Hemoptysis
- Dental Bleeds
- Red Food Colouring
- Bismuth/Iron supplements
LGI bleed mimics
- Vaginal Bleeding
- Gross Hematuria
- Red Foods (BEETS)
Glasgow Blatchford Score
Screens need for intervention - Transfusion and OGD
NOT FOR VARICEAL BLEEDS
Score
0 - Rx as OP
1-6 - should have OGD within 24 hrs
Score >6 suggest high risk bleed and 50% need intervention
7-12 - MUST have OGD within 24 hrs
>12 - MUST have ODG within 12 hours
Must have OGD in 6 hours
* suspected variceal bleed
* Unstable
* High volume
Jaundice differential
UNCONJUGATED HYPERBILIRUBINAEMIA
Pre-HEPATIC (overproduction of heme)
* Haemolysis - Haemolytic anaemias,
* Congenital - Gilberts, Crigler-Najar Syndrome
* Thalassaemia
* Trauma
* Severe CCF
* G6PD deficiency + oxidative drugs
HEPATIC (reduced hepatocyte Br uptake)
* Chronic hepatic cirrhosis
* Infection
* Viral / Bacterial / Protozoal
* Sepsis
* Drugs
* Toxins
* Alcohol
* Autoimmune
CONJUGATED HYPERBILIRIBUINAEMIA
POST-Hepatic (decreased excretion of Br)
* Hepatocellular (dec hepatocyte function)
* Hepatitis - viral, toxic, alcohol, AI
* Cirrhosis
* Drugs - paracetamol, methyldopa, pheyntoin
* Intra-hepatic
* Hepatitis
* Primary Biliary Cirrhosis
* Intrahepatic cholestasis
* Drugs - indomethacin, erythromycin, chlorproamzine, isoniazid, flucloxacillin, OCP
* Extra-hepatic
* Intraluminal - CBD stone, stenosis/ scarring PBC, PSC
* Pancreatitis
* External - Carcinoma - GB. pancreas, Ampullary
PREGNANCY
- Pre-eclampsia
- HELLP
- Acute fatty liver
- Hyperemesis gravidarum
- Cholestasis of pregnancy
Crohn’s vs UC
Bilirubin metabolism
1 Creation of Bilirubin
Reticuloendothelial cells take up RBCs
Metabolised into individual components; haem and globin. Globin broken down into amino acids which are subsequently recycled.
Haem broken down into iron and biliverdin by haem oxygenase. The iron gets recycled, while biliverdin is reduced by biliverdin reductase to create unconjugated Br.
2 – Bilirubin Conjugation
In the bloodstream, unconjugated Br binds to albumin to facilitate its transport to the liver. Once in the liver, glucuronic acid is added to unconjugated bilirubin by the enzyme glucuronyl transferase. This forms conjugated Br, which is soluble. Excreted in bile to duodenum.
3 – Bilirubin Excretion
Once in the colon, colonic bacteria deconjugate bilirubin and convert it into urobilinogen. Around 80% of this urobilinogen is further oxidised by intestinal bacteria and converted to stercobilin and then excreted through faeces. It is stercobilin which gives faeces their colour.
Around 20% of the urobilinogen is reabsorbed into the bloodstream as part of the enterohepatic circulation. It is carried to the liver where some is recycled for bile production, while a small percentage reaches the kidneys. Here, it is oxidised further into urobilin and then excreted into the urine.
Urine Dip in Biliary Disorders
Caecal vs Sigmoid Volvulus
UC - Truelove & Witt Score
