GI Flashcards
where in the oesophagus are oesophageal varices most likely
lower oesophagus and gastric cardia
also found in the stomach, around the umbilicus (caput medusae) and rectum.
name pre-hepatic causes of oesophageal varices
portal or hepatic vein thrombosis
name intra-hepatic causes of oesophageal varices
cirrhosis
schistosomiasis (developing countries)
name post-hepatic causes of oesophageal varices
right heart failure
budd-chiari syndrome
veno-occlusive disease
constrictive pericarditis
risk factors for variceal bleeds
high portal pressure
variceal size
endoscopic features of variceal bleed (e.g. haematocystic spots)
child-pugh score ≥8
prophylaxis of variceal bleeds
propranolol
endoscopic band ligation
secondary cause
- transjugular intrahepatic portal-systemic shunt (TIPSS)
acute variceal bleed management
call senior
resus until harm-dynamically stable
correct clotting abnormalities - vitamin K, FFP, platelets.
IVI TERLIPRESSIN
endoscopic band ligation or sclerotherapy 2nd line
Sengstaken-Blakemore tube - if bleeding ongoing
liver failure causes
Infections
- hepatitis B + C
- EBV
- CMV
Hereditary
- Wilsons disease
- Hereditary haemachromatosis
- Alpha 1 antitrypsin deficiency
Budd-chiari syndrome
NAFLD
alcohol fatty liver disease
Primary biliary cirrhosis
primary sclerosis cholangitis
autoimmune hepatitis
drugs
- paracetamol overdose
- isoniazid
HELLP syndrome
malignancy (HCC, cholangiocarcinoma)
signs of liver failure
jaundice
hepatic encephalopathy
fetor hepaticus (smells like pear drops)
asterixis/flap
Bloods for liver failure
FBC, U+E, LFT, Clotting, GLUCOSE
paracetamol level
hepatitis serology
cmv + ebv serology
ferritin
alpha-1-antitrypsin level
caeruloplasmin autoantibodies
imaging for liver failure
abdominal USS
DOPPLER-FLOW STUDIES TO ASSESS FOR PORTAL VEIN THROMBOSIS
management of liver failure
- Nurse with a 20° head-up tilt in ITU. Protect the airway with intubation and insert an NG tube to avoid aspiration and remove any blood from stomach.
- Insert urinary and central venous catheters to help assess fluid status.
- Monitor T°, respirations, pulse, BP, pupils, UO hourly. Daily weights.
- Check FBC, U&E, LFT and INR daily
- 10% glucose IV, 1L/12h to avoid hypoglycaemia. Do glucose every 1-4h.
- Treat the cause, if known (e.g. GI bleeds, sepsis, paracetamol poisoning)
- If malnourished, get dietary help: good nutrition can decrease mortality (e.g. carbohydrate-rich foods). Give thiamine and folate supplements.
- Treat seizures with lorazepam!
- Haemofiltration or haemodialysis if renal failure develops
- Try to avoid sedatives and other drugs with hepatic metabolism
- Consider PPI as prophylaxis against stress ulceration, e.g. omeprazole
- Liaise early with nearest transplant centre.
complications of liver failure
- Bleeding
- Ascites
- Infection - sbp
- hypoglycaemia
- encephalopathy
- cerebral oedema
factors that indicate worse prognosis in liver failure
- Grade III-IV encephalopathy
- Age >40y
- Albumin <30g/l
- High INR
- Drug-induced liver failure
- Late-onset hepatic failure worse than fulminant failure
name some hepatotoxic drugs
o Paracetamol o Methotrexate o Isoniazid o Azathioprine o Phenothiazines o Oestrogen o 6-mercaptopurine o Salicylates o Tetracycline o Mitomycin
which drugs should be avoided in patients with liver failure
opiates - cause constipation (increase risk of encephalopathy)
sedatives
oral hypoglycaemics
underlying cause of hepatic encephalopathy
liver failure causes ammonia build up in the circulation and passes to the brain.
astrocytes clear it (by processes involving the conversion of glutamate to glutamine.
excess glutamine causes an osmotic imbalance and a shift of fluid into these cells - hence cerebral oedema in liver disease.
grading of hepatic encephalopthy
o I – altered mood/behaviour; sleep disturbance (e.g. reversed sleep pattern); dysparaxia (please copy this 5 pointed star); poor arithmetic. No liver flap.
o II – increasing drowsiness, confusion, slurred speech ± liver flap, inappropriate behaviour/personality change (ask family)
o III – incoherent; restless; liver flap; stupor
o IV – coma
management of hepatic encephalopathy
lactulose ± enemas
rifaximin
triad of hepatorenal syndrome
cirrhosis + ascites + renal failure
types of hepatorenal syndrome
HRS1 - rapidly progressive deterioration in circulatory and renal function (median survival 2 weeks)
HRS2 - steady deterioration (survival about 6 months)
King’s college criteria for liver transplantation - paracetamol-induced liver failure
Paracetamol-induced liver failure
- Arterial ph <7.3 24hours after ingestion
OR ALL OF THE FOLLOWING
o PT >100sec
o Creatinine >300umol/l
o Grade III or IV encephalopathy
King’s college criteria for liver transplantation - non-paracetamol liver failure
Non-paracetamol liver failure
- PT >100sec
OR 3 OUT OF 5 THE FOLLOWING: o Drug-induced liver failure o Age <10 or >40y o >1week from 1st jaundice to encephalopathy o PT >50sec o Bilirubin ≥300umol/l
cirrhosis causes
- Chronic alcohol abuse
- HBV or HCV infection
- Genetic disorders: haemochromatosis, alpha1-antitrypsin deficiency, Wilson’s disease
- Hepatic vein events (budd-Chiari)
- Non-alcoholic steatohepatitis
- Autoimmunity: primary biliary cirrhosis; primary sclerosing cholangitis; autoimmune hepatitis
- Drugs: amiodarone, methyldopa, methotrexate
chronic liver disease signs
leukonychia - white nails with lunula demarcated, from hypoalbuminaemia.
terry’s nails - while proximally but distal 1/3 reddened by telangiectasia.
clubbing palmar erythema hyper dynamic circulation dupuytren's contracture spider naevi xanthelasma gynaecomastia atrophic testes loss of body hair parotid enlargement hepatomegaly small liver in late disease
complications of portal hypertension
ascites
splenomegaly
oesophageal varices (± life threatening upper GI bleed)
caput medusae - enlarged superficial periumbilical veins
complications of cirrhosis
coagulopathy encephalopathy hypoalbuminaemia sepsis spontaneous bacterial peritonitis hypoglycaemia hepatocellular carcinoma
management of cirrhosis
- general
o Good nutrition is vital o Alcohol abstinence o Avoid NSAIDs, sedatives and opiates o Colestyramine helps pruiritis o Consider USS and alpha-fetoprotein every 3-6m to screen for HCC
management of cirrhosis
- specific
o High-dose ursodeoxycholic acid in PBC may normalize LFT, but may have no effect on disease progression.
o Penicillamine for Wilson’s disease
management of ascites
o Bed rest, fluid restriction (<1.5l/d), low salt diet (40-100mmol/d)
o Give spironolactone
o Chart daily weight and aim for weight loss of ≤0.5kg/d
o If response is poor, add furosemide ≤120mg/24h PO; do U&E (watch Na)
o Therapeutic paracentesis with concomitant albumin infusion (6-8g/l fluid removed) may be tried.
management of spontaneous bacterial peritonitis
o MUST BE CONSIDERED IN ANY PATIENT WITH ASCITES WHO DETERIORATES SUDDENLY (MAY BE ASYMPTOMATIC)
o Common organisms – E.coli, Klebsiella and streps
o Rx
CEFOTAXIME 2g/6h or TAZOCIN 4.5g/8h for 5d or until sensitivities known (+ METRONIDAZOLE 500mg/8h IV if recent instrumentation to ascites)
o Give prophylaxis for high-risk patients (low albumin, high PT/INR, low ascitic albumin) or those with a previous episode NORFLOXACIN 400MG PO daily continued until death, transplant or ascites resolves.
definitive treatment for cirrhosis
LIVER TRANSPLANT
scoring system used to assess severity of cirrhosis
Child-Pugh score
MELD
- Assesses bilirubin, albumin, PT (seconds > normal), ascites, encephalopathy
what is hereditary haemachromastosis
Autosomal recessive disorder
- Inherited disorder of iron metabolism in which high intestinal iron absorption leads to iron deposition in joints, liver, heart, pancreas, pituitary, adrenals and skin.
- MALES > FEMALES
(menstrual blood flow is protective in women - so usually presents later in females)
major mutations in hereditary haemachromatosis
C282Y
H63D
on HFE gene (chromosome 6)
clinical presentation of hereditary haemochromatosis
TIREDNESS
ARTHRALIGIA
ERECTILE DYSFUNCTION (hypogonadism) - amenorrhoea in females
SKIN HYPERPIGMENTATION (BRONZE SKIN)
later
- SLATE-GREY SKIN PIGMENTATION
- signs of chronic liver disease
- hepatomegaly
- cirrhosis
- dilated cardiomyopathy
- osteoporosis
- DIABETES
Tests for hereditary haemochromatosis
bloods
- high iron
- high ferritin
- high transferrin saturation
- low TIBC
LFT - deranged
imaging
- x-ray - chondrocalcinosis
- liver MRI - iron overload
- liver biopsy - Perl’s stain quantifies iron loading and assesses disease seventy.
- ecg/echo - monitor cardiomyopathy
treatment of haemachromatosis
VENESECTION - 1unit/1-3 weeks, until ferritin ≤50
consider desferrioxamine if intolerant to this.
monitor LFT/GLUCOSE/HBA1C
diet - well balanced low iron diet
tea, coffee and red wine lowers iron absorption
screening - serum ferritin and genotype
causes of secondary haemachromatosis
- high number of transfusions
- red meats, liver, seafood, enriched breakfast cereals and pulses and spices (e.g. paprika) are iron-rich
iron absorption occurs mainly in the duodenum and jejunum
where does iron absorption occur
iron absorption occurs mainly in the duodenum and jejunum
what is alpha-1-antitrypsin deficiency
commonly affects lung and liver
causes emphysema and cirrhosis of the liver and hcc
AUTOSOMAL RECESSIVE - chromosome 14
what is A1AD associated with
HCC asthma pancreatitis gallstones wegener's
tests for A1AD
serum alpha-1-antitrypsin levels - low
management of A1AD
- MDT with GP, lung and liver specialists and geneticists
- Supportive treatment for emphysema and liver disease may be sufficient
- Quit smoking
- Give IV A1AT pooled from human plasma is expensive and useless according to some, but COPD exacerbations may be prevented.
- Liver transplantation – decompensated cirrhosis
- Inhaled A1AT has been tried in lung disease
which transaminase is high in alcoholic liver disease
AST > ALT
high GGT and macrocytosis
high IgA
risk factors for NAFLD
OBESITY
DM
HIGH LIPIDS
what is ischaemic hepatiits
seen in conditions where circulatory overload is low (MI, hypotension and haemorrhage)
drug-induced hepatitis - which transaminase is high
ALT > AST (in 1000s)
commonest drug causes of drug-induced hepatitis
co-amoxiclav disulfiram flucloxacillin NSAIDs carbamazepine phenytoin
test for PBC
anti-mitochondrial antibodies
high IgM
test for PSC
p-ANCA positive
test for autoimmune hepatitis
anti-smooth muscle antibodies
high IgG
what is PBC
interlobular bile ducts damaged by chronic autoimmune granulomatous inflammation causing cholestasis –> fibrosis, cirrhosis, portal hypertension
who is affected PBC the most
female patients in their 50s
presenting signs of PBC
itching jaundice XANTHELASMA/XANTHOMATA hepatosplenomegaly tiredness skin pigmentation
complications of PBC
cirrhosis
osteoporosis
malabsorption of ADEK due to cholestasis and low bilirubin in the gut lumen results in osteomalacia and coagulopathy.
vitamin A - vision, reproduction, immune system, skin
vitamin D - strengthens bones, calcium absorption, immune system
vitamin E - immune system, flushes toxins
vitamin K - blood clotting
tests for PBC
high alkaline phosphate
high GGT
mildly elevated AST and ALT
98% - AMA M2 positive
IgM high
Ultrasound liver
treatment of PBC
ursodeoxycholic acid
pruritus - colestyramine
diarrhoea - codeine
osteoporosis - calcium, vit d, bisphosphonates
ADEK supplements
liver transplant - end stage
monitor in PBC
for HCC - ultrasound and AFP levels every 6 months
regular LFTs
what is PSC
progressive cholestasis with bile duct inflammation and strictures of the intrahepatic and extra hepatic bile ducts.
presentation of PSC
pruritus
fatigue
jaundice
what is PSC associated with
IBD
cancers
- cholangiocarcinoma
- HCC
- colorectal cancer
tests for PSC
high Alk Phos
high bilirubin
ANCA positive
ERCP
biopsy of liver - fibrotic
treatment of psc
ursodeoxycholic acid
colestyramine for pruritis
antibiotics if ascending cholangitis suspected
liver transplant
what is autoimmune hepatitis
autoimmune disease of the liver causing damage to the hepatocytes.
affects young or middle-aged women (10-30y or >40y)
what are the different types of autoimmune hepatitis
I – seen in 80%. Typical patient – F <40y.
- Anti-smooth muscle antibodies (ASMA) +ve in 80%.
- Antinuclear antibody (ANA) +ve in 10%.
- IgG high in 97%
- Good response to immunosuppression in 80%
- 25% have cirrhosis at presentation
II – commoner in Europe than USA. MORE OFTEN SEEN IN CHILDREN
- MORE COMMONLY PROGRESSES TO CIRRHOSIS AND LESS TREATABLE
- ANTILIVER/KIDNEY MICROSOMAL TYPE 1 (LKM1) antibodies +ve
- ASMA and ANA -ve
III – like type I but ASMA and ANA NEGATIVE
- Antibodies against soluble liver antigen (SLA) or liver-pancreas antigen
tests for autoimmune hepatitis
serum bilirubin, AST, ALT, and alk phos all high
high IgG
Anti-smooth muscle antibody, ANA + LKM1 positive
anaemia, low WCC, low Plt - hypersplenism
liver biopsy - mononuclear infiltrate of portal and periportal areas and piecemeal necrosis ± fibrosis
management of autoimmune hepatitis
prednisolone - for 1 month
azathioprine - maintains remission
liver transplant
association of autoimmune hepatitis
pernicious anaemia UC autoimmune thyroiditis autoimmune haemolysis DM PSC glomerulonephritis
what is NAFLD
fatty liver entails high fat in hepatocytes (steatosis) ± inflammation (steatohepatitis).
typical patient for NAFLD
OBESE FEMALE - middle aged
risk factors for NAFLD
- DM
- Obesity
- dyslipidaemia
- parenteral feeding
- Wilsons disease
investigation for NAFLD
liver USS
± biopsy
management of NAFLD
control risk factors - lifestyle advice
no drug proven to benefit
what is Wilson’s disease
Wilsons disease is a rare INHERITED DISORDER OF BILIARY COPPER EXCRETION WITH TOO MUCH COPPER IN LIVER AND CNS (basal ganglia e.g. globus pallidus hypodensity ± putamen cavitation).
autosomal recessive - on chromosome 13 - ATP7B
pathophysiology of wilsons disease
In Wilsons disease, intestinal copper absorption and transport into the liver are intact, while copper incorporation into caeruloplasmin in liver and its excretion into bile are impaired. Therefore, copper accumulates in liver and later in other organs.
signs of wilsons disease
Liver disease - hepatitis, cirrhosis, fulminant liver failure.
CNS signs - tremor, dysarthria, dysphagia, dyskinesia, dystonia, hand clapping, dementia, parkinsonism, micrographia, ataxia/clumsiness.
mood - depression/mania, labile emotions, high/low libido, personality change.
cognition - low memory, quick to anger, low IQ
KAYSER-FLEISCHER RINGS – COPPER IN IRIS
other
- haemolysis
- blue nails
- arthritis
- hypermobile joints
- grey skin
difference between haemachromatosis and wilsons disease
NO CNS SIGNS WITH HAEMOCHROMATOSIS.
in wilsons disease, copper deposits in the basal ganglia causing dystonia, tremor, dyskinesia, parkinsonism.
investigation for wilsons disease
serum copper - low
serum caeruloplasmin - low
urinary copper - high
LFT - deranged
slit lamp exam - keiser-fleisher rings on iris/descemet’s membrane
liver biopsy - high hepatic copper, hepatitis, cirrhosis
MRI - degeneration in basal ganglia
management of wilsons disease
diet - avoid high copper content foods e.g. liver, chocolate, nuts, mushroom, legumes and shellfish
LIFELONG PENCILLINAMINE (can cause a pancytopenia)
alternative - Trientine dihydrochloride
most liver tumours are secondary - where do they originate from
breast
lung
GI tract - colon, stomach
benign tumours of the liver
Cysts Haemangioma – commonest benign tumour, F:M = 5:1 Adenoma Focal nodular hyperplasia Fibroma Benign GIST = leiomyoma
malignant tumours of the liver
HCC Cholangiocarcinoma Angiosarcoma Hepatoblastoma Fibrosarcoma and hepatic GI stromal tumour (GIST, formerly leiomyosarcoma)
symptoms and signs of liver cancer
fever malaise anorexia weight loss ruq pain
hepatomegaly
chronic liver disease signs
evidence of decompensation
feel for an abdominal mass
investigations for liver cancer
FBC clotting LFT hepatitis serology AFP HIGH
imaging
- CT + ultrasound to identify lesions and guide biopsy.
- ERCP if cholangiocarcinoma suspected
- biopsy
causes of HCC
HBV HCV Autoimmune hepatitis cirrhosis (alcohol, haemachromatosis, PBC) NAFLD
causes of cholangiocarcinoma
PSC (screen with CA19-9)
HBV
HCV
DM
presentation of cholangiocarcinoma
fever abdo pain ± ascites malaise high bilirubin very high alk phos
management of cholangiocarcinoma
70% are unsuited to surgery
surgery
- major hepatectomy + extrahepatic bile duct excision + caudate lobe resection.
or
to improve QOL
- stenting of an obstructed extrahepatic biliary tree, percutaneously or via ERCP
what is UC
relapsing and remitting inflammatory disorder of the colonic mucosa
what are the subtypes of UC
proctitis (rectum)
left sided colitis
pancolitis (entire colon)
Pathology of UC
hyperaemic/haemorrhagic granular colonic mucosa ± pseudo polyps formed by inflammation
punctate ulcers may extend deep into the lamina propriety - inflammation is normally not transmural
histology findings in UC
inflammatory infiltrate goblet cell DEPLETION glandular distortion mucosal ulcers CRYPT ABSCESSES
is smoking protective of uc
yes
symptoms of UC
episodic or chronic diarrhoea (± blood and mucus)
crampy abdo discomfort
bowel frequency relates to severity.
urgency/tenesmus = rectal uc
systemic symptoms in attacks - fever, malaise, anorexia, weight loss
signs of UC
acute, severe UC
- fever
tachycardia
tender, distended abdomen
extra-intestinal signs of uc
erythema nodosum episcleritis, scleritis arthralgia pyoderma gangrenosum aphthous oral ulcers PSC
sacroilitis
ankylosing spondylitis
amyloidosis
investigations for uc
BLOODS - FBC, U+E, ESR/CRP, LFT, Blood culture
stool mc&S - rule out infective cause
erect CXR - perforation
COLONOSCOPY + BIOPSY - DIAGNOSTIC
which scoring method used to assess UC severity
Truelove and Witt’s severity index
what parameters are found in truelove and witt’s index to diagnose uc
number of motions in a day rectal bleeding temperature resting HR haemoglobin ESR
complications of uc
PERFORATION HAEMORRHAGE toxic megacolon venous thrombosis colorectal cancer
first line recommended treatment for UC (proctitis + left sided colitis)
topical aminosalicylate (sulfasalazine)
second line rx for UC (proctitis) if no improvement after 4 weeks
add an oral aminosalicylate (mesalazine)
3rd line rx for UC (proctitis) if still no improvement
add a topical or oral corticosteroid for 4-8 weeks
second line rx for UC (left sided colitis) if no improvement after 4 weeks
add a high dose oral aminosalicylate
or
switch to a oral aminosalicylate + topical corticosteroid (4-8 weeks)
3rd line rx for UC (left sided colitis) if still no improvement
STOP TOPICAL TREATMENT
offer
- oral aminosalicylate +
oral corticosteroid (4-8 weeks)
first line rx for PANCOLITIS (UC)
topical aminosalicylate + oral aminosalicylate
2nd line rx for pancolitis after 4 weeks
STOP TOPICAL TREATMENT
offer
- oral aminosalicylate + oral corticosteroid (4-8 weeks)
rx for patients unsuitable for aminosalicylates in UC
give topical or an oral corticosteroid for 4-8 weeks
give oral corticosteroid in pancolitis
treatment of acute severe UC
NBM and IV fluids
IV HYDROCORTISONE or methylprednisolone
2nd line - IV ciclosporin
consider surgery in patients who do not improve with iv steroids within 72h.
maintenance of remission in UC
proctitis - rectal aminosalicylate or in combination with an oral aminosalicylate.
left sided colitis/pancolitis - low dose oral aminosalicylate
severe relapse or ≥2 exacerbations requiring steroids - oral azathioprine or oral mercaptopurine
what surgery required in UC
proctocolectomy + terminal ileostomy
what is crohn’s disease
- Chronic inflammatory GI disease characterized by TRANSMURAL GRANULOMATOUS INFLAMMATION AFFECTING ANY PART OF THE GUT FROM MOUTH TO ANUS (esp terminal ileum in 70%) and proximal colon)
- SKIP LESIONS PRESENT
does smoking increase risk of crohn’s disease
yes - x3-4
symptoms of crohn’s disease
diarrhoea/urgency
abdo pain
weight loss
fever, malaise, anorexia
signs of crohn’s disease
aphthous oral ulcers
abdo tenderness
perianal abscess/fistulae/skin tags
anal strictures
complications of crohn’s disease
small bowel obstruction toxic megacolon abscess fistulae perforation haemorrhage small intestine cancer
investigation for crohn’s disease
bloods - FBC, U+E, ESR/CRP, LFT, B12, FOLATE, IRON PROFILE, CLOTTING
stool mc&s - exclude infection
COLONOSCOPY + BIOPSY
histology for crohns disease
transmural inflammation
non-caseating granulomas
goblet cells
non-pharmacological management of crohns disease
smoking cessation
optimise nutrition - elemental diet containing amino acids
rx - first presentation of crohns disease (Acute)
ORAL PREDNISOLONE
or
IV hydrocortisone
(BUDESONIDE if distal ileal, ileocaecal or right-sided colonic disease and if steroids are C/I)
add on therapy (only if there are ≥2 inflammatory exacerbations in 1 year or the corticosteroid dose cannot be reduced):
- add azathioprine or mercaptopurine (if both c/i –> add methotrexate instead)
if inadequate response to above –> add the TNF-alpha inhibitors (adalimumab or infliximab)
maintenance therapy for crohns disease
azathioprine or mercaptopurine
2nd line - methotrexate
(DO NOT OFFER CORTICOSTEROIDS OR BUDOSENIDE)
maintenance of remission following surgery in crohns
azathioprine + metronidazole for 3 months
poor prognosis factors in crohns
onset at age <30y
steroids needed at first presentation.
perianal disease
diffuse small bowel disease
what is irritable bowel syndrome
- IBS denotes a mixed group of abdominal symptoms for which no organic cause can be found.
- Most are probably due to disorders of intestinal motility or enhanced visceral perception
- Age at onset - ≤40 years
- Female:male - ≥2:1
diagnosis of IBS
abdominal pain (or discomfort) is either relieved defecation or associated with altered stool form or bowel frequency (constipation and diarrhoea may alternate)
AND THERE ARE ≥2 OF: o URGENCY o INCOMPLETE EVACUATION o ABDO BLOATING/DISTENSION o MUCOUS PR o WORSENING OF SYMPTOMS AFTER FOOD
what criteria is required to diagnose IBS
chronic symptoms (≥6 months) exacerbated by stress, menstruation or gastroenteritis (post-infection IBS)
investigations for IBS
bloods - FBC, ESR, CRP, LFT, COELIAC SEROLOGY
if ≥50y or any marker or organic disease (high temp, blood PR, weight loss) = colonoscopy.
exclude ovarian cancer - CA125, ultrasound
o If diarrhoea is prominent do: LFT, stool culture, B12/folate, anti-endomysial antibody (coeliac), TSH
treatment for IBS
- Explanation and reassurance are vital as is interdisciplinary teamwork
- Ensure healthy diet; fibre; lactose; fructose; wheat; starch; caffeine; sorbitol
alcohol and fizzy drinks may worsen symptoms.
constipation - bisacodyl. increase fibre.
diarrhoea - loperamide after each loose stool.
colic/bloating - antispasmodics - mebeverine
consider CBT, hypnosis
what are risk factors for developing pancreatic cancer
SMOKING ALCOHOL carcinogens Diabetes chronic pancreatitis increased waist circumference
what type of carcinoma is pancreatic cancer
DUCTAL ADENOCARCINOMA
where is a common place for pancreatic cancer to arise
head of the pancreas
other
- body
- tail
- ampulla of vater
- pancreatic islet cells (insulinoma, gastrinoma)
which gene affected in pancreatic cancer
KRAS2 gene
typical presentation of pancreatic cancer
PAINLESS OBSTRUCTIVE JAUNDICE
other
- anorexia
- weight loss
- diabetes
- acute pancreatitis
signs of pancreatic cancer
JAUNDICE + PALPABLE GALLBLADDER (courvoisier’s law)
epigastric mass
hepatosplenomegaly
lymphadenopathy
ascites
investigations for pancreatic cancer
cholestatic jaundice - high GGT, high alk phos
CA19-9 level
imaging - USS or CT abdomen scan + biopsy
- shows a pancreatic mass ± dilated biliary tree ± hepatic metastases
endoscopic sonography (EUS) - most accurate for diagnosis and staging.
ERCP - shows biliary tree anatomy and may localise site of obstruction.
treatment of pancreatic cancer
pancreato-duodenectomy (whipple’s procedure)
post-op chemo
palliation of jaundice - endoscopic or percutaneous stent insertion may help jaundice and anorexia.
pain - analgesia
which vitamin lacking in scurvy
vitamin C
signs of scurvy
anorexia, cachexia gingivitis, loose teeth, foul breath bleeding from gums, nose, hair follicles or into joints, bladder, gut muscle pain and weakness oedema
treatment of scurvy
ascorbic acid
what is beriberi
lack of vitamin B1 (thiamine). wernickes causes this.
what is wet beriberi
heart failure with general oedema
what is dry beriberi
peripheral neuropathy
what is pallegra
lack of nicotinic acid.
classic triad - diarrhoea, dementia and dermatitis
- ± neuropathy, depression, insomnia, tremor, rigidity, ataxia, fits
treatment of Allegra
o Education
o Electrolyte replacement
o Nicotinamide 100mg/4h PO
what is xerophthalmia
vitamin A deficiency syndrome
big cause of BLINDNESS IN THE TROPICS
what are carcinoid tumours
tumours of enterochromaffin cells (neural crest) origin, by definition capable of producing 5HT.
80% of tumours >2cm across will metastasize (i.e. consider all as malignant).
common site for carcinoid tumour
appendix
ileum
rectum
what is carcinoid syndrome
occurs in 5% and implies hepatic involvement.
symptoms and signs of carcinoid syndrome
bronchoconstriction
paroxysmal flushing
diarrhoea
CCF
investigation for carcinoid syndrome
24-hour urine 5-hydroxyindoleacetic acid (5-HIAA) HIGH
- CXR + Chest/Pelvis MRI/CT help locate primary tumours
- ECHO and BNP – used to investigate carcinoid heart disease
treatment of carcinoid syndrome
octreotide (somatostatin analogue)
tumour resection - only cure for carcinoid tumours.
what is a carcinoid crisis
- When a tumour outgrows its blood supply or is handled too much during surgery, mediators flow out.
- Life-threatening vasodilation, hypotension, tachycardia, bronchoconstriction, and hyperglycaemia.
- TREATED WITH HIGH DOSE OCTREOTIDE, SUPPORTIVE MEASURES AND CAREFUL MANAGEMENT OF FLUID BALANCE (i.e. a central line is needed)
what are symptoms of malabsorption
diarrhoea weight loss lethargy steatorrhoea bloating
tests for malabsorption
bloods
- fbc: low or high MCV
- low calcium
- low iron
- low b12/folate
- high INR
- lipid profile
coeliac serology
stool mc&s, elastase
endoscopy + small bowel biopsy
ERCP - biliary obstruction
commonest causes of malabsorption in the UK
coeliac disease, chronic pancreatitis, crohn’s disease
what is coeliac disease
T-cell mediated AUTOIMMUNE DISEASE OF THE SMALL BOWEL.
Gliadin intolerance causes villous atrophy and malabsorption.
when is coeliac disease suspected
in those with diarrhoea + weight loss or ANAEMIA
associations of coeliac disease
HLA-DQ2 (92%)
HLA-DQ8
autoimmune disease
DERMATITIS HERPETIFORMIS
presentation of coeliac disease
steatorrhoea/smelly stools diarrhoea abdo pain bloating nausea and vomiting
weight loss
fatigue
weakness
1/3 asymptomatic
signs of coeliac disease
aphthous oral ulcers
angular stomatitis
osteomalacia
failure to thrive in children
investigations for coeliac disease
low Hb
low iron
low B12
antibodies
- anti-transglutaminase antibodies
- anti-endomysial antibodies - an IgA antibody (95% specific unless IgA deficient) - so if low IgA, can’t interpret accurately.
- alpha-gliadin antibodies
DIAGNOSTIC
- ENDOSCOPY + BIOPSY OF DUODENUM
- — intraepithelial WBCs high
- —villous atrophy
- — crypt hyperplasia
exclude coeliac in all labelled as IBS
treatment for coeliac disease
lifelong gluten free diet
rice maize soya potatoes oats and sugar are ok.
complications of coeliac disease
ANAEMIA 2° lactose intolerance GI T-cell lymphoma (rare) INCREASED RISK OF MALIGNANCY (gastric, oesophageal, bladder, breast, brain) myopathies neuropathies hyposplenism osteoporosis
symptoms of chronic pancreatitis
epigastric pain radiates to back
relieved by sitting forward
bloating
steatorrhoea
weight loss
brittle diabetes
causes of chronic pancreatitis
ALCOHOL CF haemochromatosis pancreatic duct obstruction high PTH congenital
investigations for chronic pancreatitis
ultrasound ± CT (pancreatic calcification)
AXR - speckled calcification
treatment of chronic pancreatitis
analgesia
lipase
fat-soluble vitamins
insulin - variable
surgery for unremitting pain, narcotic abuse, weight loss- pancreatectomy or pancreaticojejunostomy
complications of chronic pancreatitis
pseudocyst diabetes biliary obstruction local arterial aneurysm splenic vein thrombosis gastric varices pancreatic carcinoma
tools used to assess alcohol dependence
CAGE questionnaire
AUDIT
Alcoholic hepatitis - what are the raised parameters on bloods
AST:ALT >2 high GGT high MCV high INR high urea high WCC
low platelets - hypersplenism or toxicity
signs of severe alcoholic hepatitis
jaundice
encephalopathy
coagulopathy
treatment of alcoholic hepatitis
stop alcohol consumption
(if withdrawal - chlordiazepoxide PO or lorazepam IM)
IV pabrinex
high protein diet - prevent encephalopathy, sepsis
daily weight, LFT, U+E, INR
prednisolone 40mg/d for 5d tapered over 3 weeks if Maddrey score >31 and encephalopathy.
what is found on histology for cirrhosis (biopsy findings)
mallory bodies
neutrophil infiltrate
CNS signs of alcohol excess
wernicke’s encephalopathy
korsakoff’s - confabulation
cortical atrophy retrobulbar neuropathy seizures falls wide-based gait neuropathy
GI signs of alcohol excess
obesity d+v gastric erosions peptic ulcers varices pancreatitis cancer - oesophagus, stomach, pancreatic, mouth, liver oesophageal rupture (Boerhaave's syndrome - shock and surgical emphysema)
alcohol excess findings on bloods
high MCV, anaemia - megaloblastic anaemia due to bone marrow depression, GI bleeding, alcoholism-related folate deficiency, haemolysis, sideroblastic anaemia.
heart problems in alcoholics
arrhythmia
high BP
cardiomyopathy
sudden death
symptoms of alcohol withdrawal and time frame
starts 10-72h after last drink
- tachycardia
- hypotension
- tremor
- confusion
- seizures
- delirium tremens - hallucinations (animals crawling over skin)
pregnancy complication of alcohol excess
fetal alcohol syndrome - low iq, short palpebral fissure, absent philtrum, small eyes
management of alcohol withdrawal
admit, do BP
chlordiazepoxide (wean over 7-10d).
alternative - diazepam
long term treatment of alcohol withdrawal to prevent relapse
disulfiram
acamprosate
group therapy - AA
5 causes of abdominal distention
flatus - obstruction faeces - stool impaction fetus - pregnancy fluid - ascites fat - obesity
if ascites suspected, how to investigate
aspirate ascitic fluid (paracentesis) - cytology, culture and protein level (≥30g/l)
ultrasound abdomen
causes of ascites
malignancy infection - tb low albumin CCF pancreatitis myxedema
causes of ascites with portal hypertension
cirrhosis
budd-chiari syndrome
ivc or portal vein thrombosis
portal nodes
causes of splenomegaly with fever
infection - malaria, SBE/IE, hepatitis, EBV, CMV, TB, HIV
sarcoid
malignancy
splenomegaly with arthritis causes
sjogrens syndrome RA SLE infection - lyme disease vasculitis/behcets
splenomegaly with anaemia
sickle cell disease thalassaemia leishmaniasis leukaemia pernicious anaemia
splenomegaly with lymphadenoapthy
glandular fever
leukaemia
lymphoma
sjogrens
splenomegaly with ascites
carcinoma
portal hypertension
splenomegaly with weight loss + CNS signs
cancer
lymphoma
TB
splenomegaly with purpura
septicaemia
DIC
meningococcaemia
splenomegaly with murmur
SBE/IE
rheumatic fever
massive splenomegaly causes
malaria myelofibrosis CML gaucher's syndrome leishmaniasis
acute abdomen - clinical syndromes requiring laparotomy
rupture of organ - spleen, aorta, ectopic pregnancy
shock is the leading sign
abdo swelling
hx of trauma: blunt trauma = spleen, penetrating trauma -= liver
PERITONITIS
what is peritonitis
perforation of peptic ulcer/duodenal ulcer, diverticulum, appendix, bowel or gallbladder
signs of peritonitis
shock lying still tenderness rebound tenderness board-like abdominal rigidity guarding no bowel sounds
investigation for peritonitis
ERECT CXR - pneumoperitoneum
signs of abscess
swelling
swinging fever
high WCC
what is colic
regular waxing and waning pain
caused by muscular spasm in a hollow viscus - gut, ureter, sapling, uterus, bile duct or gallbladder
restlessness
investigation for peritonitis
bloods - abc, u&e, AMYLASE, LFT, CRP, ABG (?mesenteric ischaemia), urinalysis
imaging for peritonitis
erect CXR
AXR - may show Rigler’s sign
USS - may identify perforation or free fluid immediately
treatment of peritonitis
NBM treat shock crossmatch/ group and save blood cultures antibiotics - cefuroxime + metronidazole
analgesia
iv fluids
ECG if >50y ?AAA
causes of a medical acute abdomen
IBS MI mesenteric ischaemia acute pancreatitis leaking AAA gastroenteritis lower lobe pneumonia thyroid storm TB sickle cell crisis phaeochromocytoma
symptoms of acute appendicitis
periumbilical pain that moves to the RIF
pain precedes vomiting in surgical abodmen
general signs of acute appedicitis
tachycardia fever (low grade) 37.5-38.5 furred tongue lying still foetor ± flushing shallow breaths coughing hurts
signs of acute appendicitis
guarding
rebound + percussion tenderness
anorexia
rovsig’s sign - pain in RIF when LIF pressed.
psoas sign - RIF pain on extending hip
cope sign - pain on flexion and internal rotation of right hip
investigation for acute appendicitis
bloods - neutrophil leukocytosis, elevated CRP
if female - DO A PREGNANCY TEST
ABDO USS
CT abdo pelvis more accurate but can cause fatal delay
treatment of acute appendicitis
prompt appendicectomy
antibiotics - cefuroxime + metronidazole
laparoscopy - done in women and obese
complications of acute appendicitis
perforation
appendix mass
appendix abscess
division points of the foregut
proximal to 2nd part of duodenum
supplied by coeliac trunk
midgut division points
2nd part of duodenum to 2/3 along transverse colon
supplied by SMA
hindgut division points
1/3 along transverse colon to anus
supplied by IMA
pathology of pain in acute appendicitis
early inflammation irritates the structures and walls of the appendix - colicky pain referred to mid-abdomen
as inflammation progresses and irritates the parietal peritoneum, the somatic, lateralised pain settles at mcburney’s point (2/3 along from the umbilicus to the right ASIS)
differential diagnosis of RIF pain
ectopic pregnancy UTI mesenteric adenitis cholecystitis diverticulitis PID crohns disease perforated ulcer PID
bowel obstruction features
nausea and vomiting
colicky abdominal pain
constipation (absolute - no flatus passed)
abdominal distention
fever
tachy
faeculent vomiting - late sign (colonic fistula with proximal gut)
causes of obstruction (mechanical)
Adhesions - commonest cause in SBO
colorectal cancer
intussusception - common in children (ileocaecal valve)
hernia
volvulus- caecum and volvulus
causes of obstruction (pseudo-obstruction)
paralytic ileus - post-op likely, pancreatitis, spinal injury, low K, low Na, uraemia, peritoneal sepsis and drugs
neuropathy
hirschsprung disease
AXR findings in SBO
central gas shadows with valvulae conniventes spanning across the lumen
AXR in LBO
peripheral gas shadows proximal to the blockage (caecum)
large bowel haustra do not cross the lumen’s width
common causes of SBO
adhesions
hernia
common causes of LBO
malignancy
diverticular disease
volvulus
complications of bowel obstruction
bowel ischaemia
perforation
sepsis
management of bowel obstruction
drip and suck - give iv fluids and insert NGT
NBM
analgesia bloods - FBC, U+E, amylase AXR erect CXR catheterise to monitor fluids
if imaging inconclusive - consider early CT WITH CONTRAST
characteristic sign of sigmoid volvulus on AXR
‘coffee bean’ sign
inverted ‘u’ loop of bowel
management of sigmoid volvulus
sigmoidoscopy + insertion of a FLATUS TUBE
classic triad of stomach volvulus causing obstruction
vomiting
pain
failed attempts to pass NG tube
complications of gastric volvulus
incarceration
strangulation
risk factors for gastric volvulus
congenital
- paraoesophageal hernia
- congenital bands
- bowel malformations
- pyloric stenosis
acquired
- gastric/oesophageal surgery
investigations for gastric volvulus
erect CXR - gastric dilatation and double fluid level
treatment of gastric volvulus
acutely unwell - prompt resus and laparotomy
definition of a hernia
protrusion of a viscus or part of a viscus through a defect of the walls of its containing cavity into an abnormal position.
what is a irreducible hernia
Said to be irreducible if they cannot be pushed back into the right place.
what is a incarcerated hernia
contents of the hernial sac stuck inside by adhesions
what is an obstructed hernia
gastrointestinal hernias are obstructed if bowel contents cannot pass through them - the classical features of intestinal obstruction occur.
what is a strangulated hernia
if ischaemia occurs, the patient becomes toxic and requires urgent surgery.
femoral hernia - what is it
bowel enters the femoral canal, presenting as a mass in the upper medial thigh or above the inguinal ligament where it points down the leg, unlike an inguinal hernia which points to the groin.
who does a femoral hernia commonly affect
middle aged women and the elderly
anatomical location of femoral hernias
inferior and lateral to the pubic tubercle
treatment of femoral hernia
surgical repair
herniotomy - ligation and excision of sac
herniorrhaphy - repair of the hernial sac
what is gastroschisis
protrusion of the abdominal contents through a defect in the anterior abdominal wall to the RIGHT OF THE UMBILICUS.
protruding wall is covered by a thin ‘peel’
prompt surgical repair is performed after cautious resuscitation
what is an exomphalos (omphalocele)
abdominal contents are found outside the abdomen, covered in a 3-layer membrane consisting of a peritoneum, Wharton’s jelly and amnion.
surgical repair is less urgent than in gastroschisis as the bowel is protected by the membranes.
associated with congenital abnormalities, such as anencephaly, cardiac defects, hydrocephalus, spina bifida.
what is a direct inguinal hernia
push their way directly forward through the posterior wall of the inguinal canal, into the defect in the abdominal wall.
hesselbach’s triangle;
medial to the inferior epigastric vessels
what is indirect inguinal hernia
push through the deep internal ring, and if large, out through the external ring.
lateral to the inferior epigastric vessels
which conditions predispose to umbilical hernia
MALES > FEMALES chronic cough constipation urinary obstruction heavy lifting ascites past abdominal surgery (e.g. damage to the iliohypogastric nerve during appendicectomy)
where is the deep ring found
mid-point of the inguinal ligament
where is the superficial ring found
split in the external oblique aponeurosis just superior and medial to the pubic tubercle (the body prominence forming the medial attachment of the inguinal ligament)
relations of the inguinal canal
- Floor: inguinal ligament and lacunar ligament medially
- Roof: fibres of transversalis, internal oblique
- Anterior – external oblique aponeurosis + internal oblique for the lateral 1/3
- Posterior – laterally, transversalis fascia; medially, conjoint tendon
examination of a lump in the groin
- Look for previous scars
- Feel the other side (more common on the right)
- Examine the external genitalia
- Then ask
o Is the lump visible?
If so, ask the patient to reduce it – if he cannot, make sure it is not a scrotal lump
o Ask him to cough
Appears above and medial to pubic tubercle
o If no lump is visible, ask for a cough impulse
o Repeat examination with patient standing
how to distinguish between direct and indirect hernias
reduce the hernia and occlude the deep ring with 2 fingers.
ask the patient to cough or stand.
if the hernia can be controlled after being reduced –> INDIRECT
if the hernia still protrudes –> DIRECT
gold standard for determining type is at surgery
- direct hernia: arise media to the inferior epigastric vessels
- indirect hernia: arise lateral to the inferior epigastric vessels
treatment of inguinal hernias
weight loss
smoking cessation
laparoscopic repairs
- transabdominal pre-peritoneal (TAPP)
- totally extraperitoneal (TEP)
when is return to work advised for patients with inguinal hernias
advise 4 weeks rest and convalescence over 10 weeks
what are the contents of the inguinal canal in a male
- Spermatic cord
o Vas deferens, obliterated processus vaginalis, and lymphatics
o Arteries to the vas, cremaster and testis
o Pampiniform plexus and the venous equivalent of the above
o Genital branch of the genitofemoral nerve and sympathetic nerves - Ilioinguinal nerve, which enters the inguinal canal via the anterior wall and runs anteriorly to the cord
what are the contents of the inguinal canal in a female
the round ligament of the uterus
what type of cancer is a colorectal cancer
adenocarcinoma
affects >60 year olds
predisposing factors to colorectal cancer
neoplastic polyps IBD genetic - FAP + HNPCC diet - low fibre, increased red and processed meats excessive alcohol smoking previous cancer
how to prevent colorectal cancer
aspirin - thought to inhibit polyp growth
presenting features of colorectal cancer- left-sided
bleeding/mucus PR
altered bowel habit or obstruction
tenesmus
mass PR
weight loss
fever, night sweats
perforation
haemorrhage
fistula
presenting features of colorectal cancer- right-sided
weight loss
low Hb
abdominal pain
obstruction less likely
investigations for colorectal cancer
FBC - microcytic anaemia
faecal immunochemical test (FIT)
COLONOSCOPY + BIOPSY
CT/MRI
CEA - used to monitor disease and effectiveness of treatment
dukes staging for colorectal cancer
A – limited to muscularis mucosae – 95% 5y survival
B – extension through muscularis mucosae – 77%
C – involvement of regional lymph nodes – 48%
D – distant metastases – 6.6%
treatment of colorectal cancer
surgery - removal depends on where the lesion is:
- RIGHT HEMICOLECTOMY
o Caecal, ascending or proximal transverse colon tumours - LEFT HEMICOLECTOMY
o Tumours in distal transverse or descending colon - SIGMOID COLECTOMY
o For sigmoid tumours - ANTERIOR RESECTION for low sigmoid or high rectal tumours
- ABDOMINO-PERINEAL (AP) RESECTION
o Tumours low in the rectum (≤8cm from anus): permanent colostomy and removal of rectum and anus. - HARTMANN’S PROCEDURE
o Emergency bowel obstruction, perforation or palliation
adjuvant chemotherapy used.
radiotherapy used in palliation of colon cancer.
is there screening available to detect colorectal cancer
all 60-74 year olds are sent a faecal immunochemical test (FIT) home-kit every 2 years automatically.
if it is positive - further imaging with colonoscopy is offered.
what are different types of polyps found in the bowel
- INFLAMMATORY
o UC, crohns, lymphoid hyperplasia - HAMARTOMATOUS
o Juvenile polyps
o Peutz-Jeghers - NEOPLASTIC
o Tubular or villous adenomas
o Malignant potential esp. if >2cm
- Polyps should be biopsied and removed if they show malignant change
- Most can be reached by flexible colonoscope
what type of cancer is a stomach cancer
adenocarcinomas
presentation of stomach cancer
non-specific
dyspepsia weight loss vomiting dysphagia anaemia
signs of stomach cancer
large left supraclavicular (Virchow’s node) = Troisier’s sign
acanthosis nigricans
epigastric mass
hepatomegaly
jaundice
ascites
investigation for stomach cancer
Gastroscopy + multiple ulcer edge biopsies
- AIM TO BIOPSY ALL GASTRIC ULCERS AS EVEN MALIGNANT ULCERS MAY APPEAR TO HEAL ON DRUG TREATMENT.
- Endoscopic ultrasound – evaluate depth of invasion
- CT/MRI – staging
treatment for stomach cancer
partial gastrectomy - may suffice for distal tumours
total gastrectomy - more proximal tumours
adjuvant chemotherapy
risk factors for developing oesophagus cancer
ALCOHOL excess smoking diet achalasia plummer-vinson syndrome obesity reflux oesophagitis ± barrett's oesophagus
which type of cancer affects the distal oesophagus
ADENOCARCINOMA
which type of cancer affects the proximal oesophagus
SQUAMOUS CELL CARCINOMA
presentation of oesophagus cancer
dysphagia
dysphonia (hoarse voice)
dyspnoea (airway obstruction)
weight loss
retrosternal chest pain
investigation for oesophagus cancer
OGD with biopsy
staging for oesophagus cancer
- Spread of eosophageal cancer is direct, by submucosal infiltration and local spread -or to nodes, or later, via blood.
- Tis – carcinoma in situ
o T1 – invading lamina propria/submucosa
o T2 – invading muscularis propria
o T3 – invading adventitia
o T4 – invasion of adjacent structures - Nx – nodes cannot be assessed
o N0 – no nodes spread
o N1 – regional node metastases - M0 – no distant spread
o M1 – distant metastases
management of oesophagus cancer
if localised T1/T2 - radical curative oesophagectomy
cause of oesophageal rupture
iatrogenic - endoscopy/biopsy/dilatation (85-90%)
trauma - penetrating injury/ingestion of foreign body
carcinoma
boerhaave syndrome - rupture due to violent vomiting
corrosive ingestion
clinical features of oesophageal rupture
odynophagia
tachypnoea
dyspnoea
fever
shock
surgical emphysema - crackling sensation felt on palpating skin over the chest or neck caused by air tracking from the lungs.
treatment of oesophageal rupture
iatrogenic perforations are less prone to mediastinitis and sepsis and may be managed conservatively with NGT, PPI and Abx
others require resuscitation, PPI, Abx, antifungals, and surgery.
what is a major risk factor for a cholangiocarcinoma
PSC
management of cholangiocarcinoma
surgical resection
if palliative - biliary stenting and chemotherapy
what must you consider in a patient presenting with abdominal pain who has AF
mesenteric ischaemia
what is acute mesenteric ischaemia
Almost always involves the SMALL BOWEL and may follow SMA THROMBOSIS OR EMBOLISM, MESENTERIC VEIN THROMBOSIS, OR NON-OCCLUSIVE DISEASE.
what is the cause of acute mesenteric ischaemia
Arterial thrombus or an embolic event would cause it
presenting symptoms of acute mesenteric ischaemia
acute severe abdominal pain
no abdominal signs
rapid hypovolaemia –> shock
investigations for acute mesenteric ischaemia
high lactate high WCC persistent metabolic acidosis high Hb modestly raised plasma amylase
imaging for acute mesenteric ischaemia
CT/MRI angiography
arteriography
ECG
treatment of acute mesenteric ischaemia
ABCDE resuscitation with - IV fluids - IV Abx (gentamicin + metronidazole) - LMWH
surgery - remove necrotic bowel (laparotomy)
ITU
what is chronic mesenteric ischaemia
‘Intestinal angina’
triad of chronic mesenteric ischaemia
severe, colicky post-prandial abdominal pain (‘gut claudication’)
weight loss
upper abdominal bruit
+PR bleeding, malabsorption, n+v
cause of chronic mesenteric ischaemia
vascular disease (95% due to diffuse atherosclerotic disease in all 3 mesenteric arteries)
investigations for chronic mesenteric ischaemia
CT angiography and contrast enhanced MR angiography
doppler USS
treatment for chronic mesenteric ischaemia
surgery considered - risk of ongoing risk of acute infarction.
what is ischaemic colitis
low flow in the inferior mesenteric artery territory
ranges from mild ischaemia to gangrenous colitis
presentation of ischaemic colitis
lower left-sided abdo pain
bloody diarrhoea
investigation for ischaemic colitis
colonoscopy + biopsy - gold standard
barium enema - shows characteristic ‘thumb’ printing of submucosal swelling
treatment for ischaemic colitis
conservative - fluids and abx
gangrenous ischaemic colitis (presents with peritonitis and hypovolaemic shock) requires prompt resuscitation followed by resection of the affected bowel and stoma formation.
what are the physical complications of gastrectomy and peptic ulcer surgery
recurrent ulceration
abdominal fullness- feeling of early satiety (±discomfort + detention) improving with time. advise small, frequent meals.
afferent loop syndrome - post-gastrectomy. afferent loop may fill with bile after a meal, causing upper abdo pain and billous vomiting.
diarrhoea
gastric tumour - as reduced acid production
high amylase
metabolic complications of gastric surgery
dumping syndrome - fainting and sweating after eating due to food of high osmotic potential being dumped in the jejunum, causing hypovolaemia from rapid fluid shifts.
weight loss - poor calorie intake
bacterial overgrowth ± malabsorption may occur
anaemia - lack of iron
osteomalacia
complications of peptic ulcer disease
perforation
haemorrhage - controlled endoscopically by adrenaline injection, diathermy, laser coagulation or heat probe.
pyloric stenosis - late complication of duodenal ulcers due to scarring.
tx - endoscopic balloon dilatation followed by maximal acid suppression.
(hypokalaemic, hypocholaraemic metabolic alkalosis)
what is severe obesity associated with
T2DM hypertension IHD sleep apnoea osteoarthritis depression
indications for bariatric surgery
BMI ≥40 or ≥35 with significant comorbidities that could improve with weight loss.
failure of non-surgical management to achieve and maintain clinically beneficial weight loss for 6months
fitness for surgery and anaesthesia
as part of an integrated programme that provides guidance on diet, physical activity and psychological concerns, as well as lifelong medical monitoring.
patient must be well informed and motivated.
if BMI ≥50, surgery is first line treatment.
what are the 2 main mechanisms by which bariatric surgery help reduce weight
- restriction of calorie intake by reducing stomach capacity.
- malabsorption of nutrients by reducing the length of functioning small bowel
2 main procedures in bariatric surgery
laparoscopic adjustable gastric banding (LAGB)
- restrictive technique creates a pre-stomach pouch by placing a silicone band around top of stomach - serves as a new smaller stomach.
Roux-en-Y gastric bypass
- portion of the jejunum is attached to a small pouch to allow food to bypass the distal stomach, duodenum, and proximal jejunum.
presentation of pyloric stenosis in child
first 3-8 weeks
projectile vomiting
M:F 4:1
baby is malnourished and always hungry
investigation for pyloric stenosis
ultrasound abdomen - hypertrophied pylorus muscle
examination findings of pyloric stenosis
palpate the olive-shaped pyloric mass in the RUQ during feed.
visible gastric peristalsis starts in the LUQ
cardinal electrolyte + ABG finding in pyloric stenosis
hypocholaraemic, hypokalaemic metabolic alkalosis
treatment for pyloric stensosi
ramstedt’s pyloromyotomy
presentation of intussusception in paediatrics
typical age - 5-12months
episodic intermittent inconsolable crying.
drawing up of legs (colic)
billous vomiting
REDCURRANT STOOLS (blood PR)
diagnosis of intussusception
sausage shaped mass on palpation
may become shocked
USS abdomen - target sign
management of intussusception
resuscitation first - iv fluids, crossmatch and pass NGT
USS with reduction by air enema or pneumatic reduction under radiographic control.
surgery - if above doesn’t work
presentation of midgut rotation in paediatrics
dark green bilious vomiting
distention
rectal bleeding
imaging for malrotation in children
upper GI contrast study - barium swallow
treatment of malrotation in children
resuscitation
surgery - broadening mesentery and untwisting bowel
what are diverticula
a GI diverticulum is an out pouching of the gut wall, usually at sites of entry of perforating arteries.
what are the 3 types of diverticular disease
Diverticulosis – diverticula are present
Diverticular disease – implies that the diverticula are symptomatic
Diverticulitis – inflammation of a diverticulum
where is the most common site for diverticulae
sigmoid colon
underlying pathology of diverticular disease
lack of dietary fibre is thought to lead to high intraluminal pressures which force the mucosa to herniate through the muscle layers of the gut at weak points adjacent to penetrating vessels.
presenting features of diverticular disease
altered bowel habit ± left-sided colic relieved by defecation.
nausea
flatulence
features of diverticulitis
altered bowel habit
nausea
flatulence
pyrexia high WCC high CRP/ESR tender colon ± localised or generalised peritoneum
diagnosis of diverticular disease
CT ABDOMEN - gold standard to confirm acute diverticulitis.
ERECT CXR - ?perforation
DONT DO COLONOSCOPY ACUTELY - RISK PERFORATION
treatment of diverticulitis
analgesia NBM IV fluids antibiotics CT-guided percutaneous drainage if abscess
complications of diverticulitis
perforation haemorrhage fistulae - enterocoelic, colovaginal, colovesicle abscess post-infective strictures
management of haemorrhage - diverticulitis
ABCDE
bloods - FBC, U+E, LFT, clotting, amylase, CRP, Group and save.
imaging - erect CXR, AXR
insert 2 wide bore cannulae
give crystalloid as replacement and maintainance iv
blood transfusion is rare.
insert urinary catheter
antibiotics - if sepsis/perforation - cefuroxime + metronidazole IV
consider omeprazole iv
keep bedbound - large bleed can occur resulting in collapse on walking.
start stool chart - mc&s
diet - clear fluids
surgery
indication - unremitting, massive bleeding
bleeding usually stops with bed rest.
if not, embolisation or colonic resection may be necessary after locating bleeding points by angiography or colonoscopy
what is angiodysplasia
submucosal arteriovenous malformations
typically present as FRESH PR BLEEDING IN ELDERLY.
pathology of angiodysplasia
70-90% lesions occur in right colon, though angiodysplasia can affect anywhere in GI tract.
diagnosis of angiodysplasia
PR examination + colonoscopy - to exclude other diagnoses.
mesenteric angiography - useful in diagnosing angiodysplasia (shows early filling at the lesion site, then extravasation).
CT angiography is an alternative
treatment of angiodysplasia
embolisation
endoscopic laser electrocoagulation
resection
causes of rectal bleeding
diverticulitis colorectal cancer haemorrhoids IBD perianal disease angiodysplasia ischaemic colitis
perianal disease - pruritus ani causes
itch occurs if the anus is moist/soiled; fissures, incompetence, poor hygiene, tight pants, threadworm, fistula, dermatoses, lichen sclerosis, anxiety, contact dermatitis.
treatment of pruritus ani
careful hygiene anaesthetic cream moist-wipe post defecation no spicy food no steroid/antibiotic cream capsaicin may help
what are the causes of fissure-in-ano
most are due to hard faeces/constipation.
usually a painful tear in the squamous lining of the lower anal canal - often, if chronic, with a ‘sentinel pile’ or mucosal tag at the external aspect.
rare causes of fissures
syphilis herpes trauma crohns anal cancer psoriasis
treatment of fissures
5% lidocaine ointment + GTN ointment or topical diltiazem (CCB)
increased dietary fibre, fluids ± stool softener and hygiene advice.
botulinum toxin injection (2nd line) and topical diltiazem.
surgery - lateral partial internal sphincterotomy
what is a fistula-in-ano
track communicates between the skin and anal canal/rectum
pathophysiology of fistula-in-ano
blockage of deep intramuscular gland ducts is thought to predispose to the formation of abscesses which discharge to form the fistulae
causes of fistula-in-ano
perianal sepsis abscesses crohn's disease TB diverticular disease rectal carcinoma immunocompromise
investigation for fistula-in-ano
MRI
endoanal US scan
treatment of fistula-in-ano
fistulotomy + excision
where are anorectal abscesses most likely and rx
perianal (45%)
ischiorectal (30%)
intersphincteric (20%)
supralevator (5%)
rx - incise and drain under GA
causes of anorectal abscesses
DM
crohn’s
malignancy
fistulae
what is a pilonidal sinus
obstruction of natal cleft hair follicles approx 6cm above the anus
INGROWING OF HAIR EXCITES A FOREIGN BODY REACTION AND MAY cause secondary tracks to open laterally ± abscesses, with foul-smelling discharge.
who is a pilonidal sinus more common in
males
obese caucasians
asia, middle east and mediterranean at high risk
treatment of a pilonidal sinus
excision of sinus tract ± primary closure.
offer hygiene and hair removal advice
causes of rectal prolapse
lax sphincter
prolonged straining
related to chronic neurological and psychological disorders.
treatment of rectal prolapse
fix rectum to sacrum (rectopexy) ± mesh insertion ± rectosigmoidectomy
treatment of perianal warts (condylomata acuminata)
podophyllotoxin or imiquimod
OR
cryotherapy/surgical excision
what is proctalgia fugax and treatment
idiopathic, intense, brief, stabbing/crampy rectal pain.
worse at night.
rx - reassurance. inhaled salbutamol or topical GTN or topical diltiazem may help
what type of cancer is an anal cancer
squamous cell (85%)
anal margin tumours - well differentiated, keratinising lesions with a good prognosis.
anal canal tumours - arise above the dentate line, poorly differentiated, non-keratinising with a poorer prognosis.
risk factors for anal cancer
HPV 16, 6, 11, 18, 31, 33
syphilis
anoreceptive homosexuals
presentation of anal cancer
bleeding pain bowel habit change pruritus ani masses stricture
treatment of anal cancer
chemo-irradiation (inc radiotherapy)
what are haemorrhoids
disrupted, dilated anal cushions.
- The effects of gravity (our erect posture), increased anal tone (?stress) and the effects of straining at stool may make the anal cushions (spongy vascular tissue) both bulky and loose and so to protrude to form piles.
o Vulnerable to trauma (e.g. from hard stools) and bleed readily from the capillaries of the underlying lamina propria —-> haemorrhoids.
why do internal haemorrhoids not cause pain
As there are no sensory fibres above the dentate line (squamomucosal junction), piles are not painful unless they thrombose when they protrude and are gripped by anal sphincter, blocking venous return
causes of haemorrhoids
constipation with prolonged straining.
congestion from a pelvic tumour
pregnancy
CCF
portal hypertension
classification of haemorrhoids
o 1st degree – remain in the rectum
o 2nd degree – prolapse through the anus on defecation but spontaneously reduce.
o 3rd degree – as for 2nd degree but require digital reduction
o 4th degree – remain persistently prolapsed
symptoms of haemorrhoids
bright red rectal bleeding
mucuous discharge
pruritus ani
severe anaemia may occur
no pain usually unless thrombosed.
investigation for haemorrhoids
PR EXAM
abdominal examination
proctoscopy - internal haemorrhoids
treatment for haemorrhoids
first line managment
- increased fluid intake and fibre is key
- topical analgesia and stool softener
non-operative management if medical management failed
- rubber band ligation
- sclerosants
- infra-red coagulation
- cryotherapy - not recommended but last resort.
surgery (4th degree)
- excisional haemorrhoidectomy (most effective)
- stapled haemorrhoidoplexy
management of prolapsed, thrombosed piles
treat with analgesia, ice packs, and stool softeners.
what is bile composed of
cholesterol
bile pigments
phospholipids
what is a pigmented gallstone
small, friable and irregular
cause is haemolysis
what is a cholesterol gallstone
large, often solitary causes - male - age - obesity
what is a mixed gallstone
calcium stones, pigment and cholesterol
what is acute cholecystitis
inflammation of the gallbladder - may cause continuous epigastric or RUQ pain (referred to right shoulder), vomiting, fever, local peritonism, or a gallbladder mass.
common sign in acute cholecystitis
MURPHY’S SIGN – lay 2 fingers over the RUQ; ask patient to breath in. This causes pain and arrest of inspiration as an inflamed GB impinges on your finger.
- Only positive if the same test in the LUQ does not cause pain
tests for acute cholecystitis
- High WCC
- ULTRASOUND
o Thick-walled, shrunken GB, pericholecystic fluid, stones, CBD (dilated if >6mm)
treatment for acute cholecystitis
NBM
analgesia
IV fluids
antibiotics e.g. cefuroxime
<1 week - laparoscopic cholecystectomy
complications of gallstones
- In the gallbladder and cystic duct o Biliary colic o Acute and chronic cholecystitis o Mucocele o Empyema o Carcinoma o Mirizzi’s syndrome - In the bile ducts o Obstructive jaundice o Cholangitis o Pancreatitis - In the gut o Gallstone ileus
what is acute pancreatitis
Self-perpetuating pancreatic inflammation by enzyme-mediated autodigestion.
- Oedema and fluid shifts cause hypovolaemia, as extracellular fluid is trapped in the gut, peritoneum, and retroperitoneum (worsened by vomiting).
- Progression may be rapid – from mild oedema to necrotising pancreatitis
causes of acute pancreatitis
- Gallstones
- Ethanol (alcohol)
- Trauma
- Steroids
- Mumps
- Autoimmune (PAN)
- Scorpion venom
- Hyperlipidaemia, hypothermia, hypercalcaemia
- ERCP and emboli
- Drugs
symptoms of acute pancreatitis
- Gradual or sudden severe epigastric or central abdominal pain (radiates to back, sitting forward may relieve)
- VOMITING
signs of acute pancreatitis
- May be mild in severe disease
- Tachycardia
- Fever
- Jaundice
- Shock
- Ileus
- Rigid abdomen
- ± local/general tenderness
Periumbilical bruising (Cullen’s sign) & Flank bruising (Grey Turner’s sign) from blood vessel autodigestion and retroperitoneal haemorrhage.
tests for acute pancreatitis
serum amylase
serum lipase
ABG
erect CXR
USS - screening for gallstones
CT abdomen - standard choice of imaging
score used to assess severity of acute pancreatitis
Glasgow criteria
≥3 positive factors detected within 48h of onset suggest severe pancreatitis and should prompt transfer to ITU/HDU. (mneomonic – PANCREAS) • PaO2 - <8kPa • Age - >55y • Neutrophilia – WBC >15 • Calcium - <2mmol/l • Renal function – urea >16 • Enzymes – LDH >600; AST >200 • Albumin - <32g/L (serum) • Sugar – glucose >10mmol/l
treatment of acute pancreatitis
NBM IV fluids to counter 3rd space losses of fluid. insert urinary catheter analgesia - pethidine IM or morphine nutrition
- Hourly pulse, BP and UO; daily FBC, U&E, Calcium, glucose, amylase, ABG
- If worsening: ITU, oxygen if low PaO2.
- In suspected abscess formation or pancreatic necrosis (on CT), consider PARENTERAL NUTRITION ± LAPAROTOMY & DEBRIDEMENT
- Antibiotics may help in specific severe disease e.g. imipenem if >30% necrosis
- ERCP + gallstone removal – for progressive jaundice
- Repeat imaging (CT) performed in order to monitor progress
early complications of acute pancreatitis
shock ARDS renal failure DIC sepsis low calcium high glucose
late complications of acute pancreatitis
pancreatic necrosis pseudocyst abscess bleeding thrombosis fistulae recurrent oedematous pancreatitis
