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Finals > GI > Flashcards

GI Flashcards

1
Q

where in the oesophagus are oesophageal varices most likely

A

lower oesophagus and gastric cardia

also found in the stomach, around the umbilicus (caput medusae) and rectum.

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2
Q

name pre-hepatic causes of oesophageal varices

A

portal or hepatic vein thrombosis

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3
Q

name intra-hepatic causes of oesophageal varices

A

cirrhosis

schistosomiasis (developing countries)

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4
Q

name post-hepatic causes of oesophageal varices

A

right heart failure
budd-chiari syndrome
veno-occlusive disease
constrictive pericarditis

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5
Q

risk factors for variceal bleeds

A

high portal pressure
variceal size
endoscopic features of variceal bleed (e.g. haematocystic spots)
child-pugh score ≥8

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6
Q

prophylaxis of variceal bleeds

A

propranolol
endoscopic band ligation

secondary cause
- transjugular intrahepatic portal-systemic shunt (TIPSS)

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7
Q

acute variceal bleed management

A

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

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8
Q

liver failure causes

A

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)

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9
Q

signs of liver failure

A

jaundice
hepatic encephalopathy
fetor hepaticus (smells like pear drops)
asterixis/flap

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10
Q

Bloods for liver failure

A

FBC, U+E, LFT, Clotting, GLUCOSE

paracetamol level
hepatitis serology
cmv + ebv serology

ferritin
alpha-1-antitrypsin level
caeruloplasmin autoantibodies

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11
Q

imaging for liver failure

A

abdominal USS

DOPPLER-FLOW STUDIES TO ASSESS FOR PORTAL VEIN THROMBOSIS

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12
Q

management of liver failure

A
  • 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.
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13
Q

complications of liver failure

A
  • Bleeding
  • Ascites
  • Infection - sbp
  • hypoglycaemia
  • encephalopathy
  • cerebral oedema
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14
Q

factors that indicate worse prognosis in liver failure

A
  • Grade III-IV encephalopathy
  • Age >40y
  • Albumin <30g/l
  • High INR
  • Drug-induced liver failure
  • Late-onset hepatic failure worse than fulminant failure
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15
Q

name some hepatotoxic drugs

A 
o	Paracetamol
o	Methotrexate
o	Isoniazid
o	Azathioprine
o	Phenothiazines
o	Oestrogen 
o	6-mercaptopurine
o	Salicylates 
o	Tetracycline
o	Mitomycin
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16
Q

which drugs should be avoided in patients with liver failure

A

opiates - cause constipation (increase risk of encephalopathy)

sedatives

oral hypoglycaemics

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17
Q

underlying cause of hepatic encephalopathy

A

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.

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18
Q

grading of hepatic encephalopthy

A

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

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19
Q

management of hepatic encephalopathy

A

lactulose ± enemas

rifaximin

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20
Q

triad of hepatorenal syndrome

A

cirrhosis + ascites + renal failure

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21
Q

types of hepatorenal syndrome

A

HRS1 - rapidly progressive deterioration in circulatory and renal function (median survival 2 weeks)

HRS2 - steady deterioration (survival about 6 months)

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22
Q

King’s college criteria for liver transplantation - paracetamol-induced liver failure

A

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

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23
Q

King’s college criteria for liver transplantation - non-paracetamol liver failure

A

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
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24
Q

cirrhosis causes

A
  • 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
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25
Q

chronic liver disease signs

A

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
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26
Q

complications of portal hypertension

A

ascites

splenomegaly

oesophageal varices (± life threatening upper GI bleed)

caput medusae - enlarged superficial periumbilical veins

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27
Q

complications of cirrhosis

A 
coagulopathy
encephalopathy
hypoalbuminaemia
sepsis
spontaneous bacterial peritonitis
hypoglycaemia
hepatocellular carcinoma
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28
Q

management of cirrhosis

- general

A 
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
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29
Q

management of cirrhosis

- specific

A

o High-dose ursodeoxycholic acid in PBC may normalize LFT, but may have no effect on disease progression.
o Penicillamine for Wilson’s disease

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30
Q

management of ascites

A

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.

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31
Q

management of spontaneous bacterial peritonitis

A

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.

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32
Q

definitive treatment for cirrhosis

A

LIVER TRANSPLANT

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33
Q

scoring system used to assess severity of cirrhosis

A

Child-Pugh score
MELD
- Assesses bilirubin, albumin, PT (seconds > normal), ascites, encephalopathy

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34
Q

what is hereditary haemachromastosis

A

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)
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35
Q

major mutations in hereditary haemachromatosis

A

C282Y
H63D

on HFE gene (chromosome 6)

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36
Q

clinical presentation of hereditary haemochromatosis

A

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
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37
Q

Tests for hereditary haemochromatosis

A

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
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38
Q

treatment of haemachromatosis

A

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

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39
Q

causes of secondary haemachromatosis

A
  • 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

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40
Q

where does iron absorption occur

A

iron absorption occurs mainly in the duodenum and jejunum

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41
Q

what is alpha-1-antitrypsin deficiency

A

commonly affects lung and liver

causes emphysema and cirrhosis of the liver and hcc

AUTOSOMAL RECESSIVE - chromosome 14

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42
Q

what is A1AD associated with

A 
HCC
asthma
pancreatitis
gallstones
wegener's
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43
Q

tests for A1AD

A

serum alpha-1-antitrypsin levels - low

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44
Q

management of A1AD

A
  • 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
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45
Q

which transaminase is high in alcoholic liver disease

A

AST > ALT

high GGT and macrocytosis

high IgA

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46
Q

risk factors for NAFLD

A

OBESITY
DM
HIGH LIPIDS

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47
Q

what is ischaemic hepatiits

A

seen in conditions where circulatory overload is low (MI, hypotension and haemorrhage)

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48
Q

drug-induced hepatitis - which transaminase is high

A

ALT > AST (in 1000s)

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49
Q

commonest drug causes of drug-induced hepatitis

A 
co-amoxiclav
disulfiram
flucloxacillin
NSAIDs
carbamazepine
phenytoin
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50
Q

test for PBC

A

anti-mitochondrial antibodies

high IgM

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51
Q

test for PSC

A

p-ANCA positive

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52
Q

test for autoimmune hepatitis

A

anti-smooth muscle antibodies

high IgG

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53
Q

what is PBC

A

interlobular bile ducts damaged by chronic autoimmune granulomatous inflammation causing cholestasis –> fibrosis, cirrhosis, portal hypertension

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54
Q

who is affected PBC the most

A

female patients in their 50s

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55
Q

presenting signs of PBC

A 
itching
jaundice 
XANTHELASMA/XANTHOMATA
hepatosplenomegaly
tiredness
skin pigmentation
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56
Q

complications of PBC

A

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

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57
Q

tests for PBC

A

high alkaline phosphate
high GGT
mildly elevated AST and ALT

98% - AMA M2 positive
IgM high

Ultrasound liver

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58
Q

treatment of PBC

A

ursodeoxycholic acid

pruritus - colestyramine
diarrhoea - codeine
osteoporosis - calcium, vit d, bisphosphonates

ADEK supplements

liver transplant - end stage

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59
Q

monitor in PBC

A

for HCC - ultrasound and AFP levels every 6 months

regular LFTs

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60
Q

what is PSC

A

progressive cholestasis with bile duct inflammation and strictures of the intrahepatic and extra hepatic bile ducts.

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61
Q

presentation of PSC

A

pruritus
fatigue
jaundice

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62
Q

what is PSC associated with

A

IBD

cancers

  • cholangiocarcinoma
  • HCC
  • colorectal cancer
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63
Q

tests for PSC

A

high Alk Phos
high bilirubin
ANCA positive

ERCP
biopsy of liver - fibrotic

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64
Q

treatment of psc

A

ursodeoxycholic acid
colestyramine for pruritis
antibiotics if ascending cholangitis suspected

liver transplant

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65
Q

what is autoimmune hepatitis

A

autoimmune disease of the liver causing damage to the hepatocytes.

affects young or middle-aged women (10-30y or >40y)

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66
Q

what are the different types of autoimmune hepatitis

A

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

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67
Q

tests for autoimmune hepatitis

A

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

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68
Q

management of autoimmune hepatitis

A

prednisolone - for 1 month
azathioprine - maintains remission

liver transplant

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69
Q

association of autoimmune hepatitis

A 
pernicious anaemia
UC
autoimmune thyroiditis
autoimmune haemolysis
DM
PSC
glomerulonephritis
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70
Q

what is NAFLD

A

fatty liver entails high fat in hepatocytes (steatosis) ± inflammation (steatohepatitis).

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71
Q

typical patient for NAFLD

A

OBESE FEMALE - middle aged

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72
Q

risk factors for NAFLD

A
  • DM
  • Obesity
  • dyslipidaemia
  • parenteral feeding
  • Wilsons disease
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73
Q

investigation for NAFLD

A

liver USS

± biopsy

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74
Q

management of NAFLD

A

control risk factors - lifestyle advice

no drug proven to benefit

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75
Q

what is Wilson’s disease

A

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

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76
Q

pathophysiology of wilsons disease

A

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.

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77
Q

signs of wilsons disease

A

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
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78
Q

difference between haemachromatosis and wilsons disease

A

NO CNS SIGNS WITH HAEMOCHROMATOSIS.

in wilsons disease, copper deposits in the basal ganglia causing dystonia, tremor, dyskinesia, parkinsonism.

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79
Q

investigation for wilsons disease

A

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

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80
Q

management of wilsons disease

A

diet - avoid high copper content foods e.g. liver, chocolate, nuts, mushroom, legumes and shellfish

LIFELONG PENCILLINAMINE (can cause a pancytopenia)

alternative - Trientine dihydrochloride

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81
Q

most liver tumours are secondary - where do they originate from

A

breast
lung
GI tract - colon, stomach

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82
Q

benign tumours of the liver

A 
	Cysts
	Haemangioma – commonest benign tumour, F:M = 5:1
	Adenoma 
	Focal nodular hyperplasia 
	Fibroma 
	Benign GIST = leiomyoma
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83
Q

malignant tumours of the liver

A 
	HCC
	Cholangiocarcinoma 
	Angiosarcoma
	Hepatoblastoma 
	Fibrosarcoma and hepatic GI stromal tumour (GIST, formerly leiomyosarcoma)
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84
Q

symptoms and signs of liver cancer

A 
fever
malaise
anorexia
weight loss
ruq pain

hepatomegaly
chronic liver disease signs
evidence of decompensation
feel for an abdominal mass

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85
Q

investigations for liver cancer

A 
FBC
clotting
LFT
hepatitis serology
AFP HIGH

imaging

  • CT + ultrasound to identify lesions and guide biopsy.
  • ERCP if cholangiocarcinoma suspected
  • biopsy
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86
Q

causes of HCC

A 
HBV
HCV
Autoimmune hepatitis
cirrhosis (alcohol, haemachromatosis, PBC)
NAFLD
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87
Q

causes of cholangiocarcinoma

A

PSC (screen with CA19-9)
HBV
HCV
DM

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88
Q

presentation of cholangiocarcinoma

A 
fever
abdo pain ± ascites
malaise 
high bilirubin
very high alk phos
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89
Q

management of cholangiocarcinoma

A

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

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90
Q

what is UC

A

relapsing and remitting inflammatory disorder of the colonic mucosa

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91
Q

what are the subtypes of UC

A

proctitis (rectum)
left sided colitis
pancolitis (entire colon)

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92
Q

Pathology of UC

A

hyperaemic/haemorrhagic granular colonic mucosa ± pseudo polyps formed by inflammation

punctate ulcers may extend deep into the lamina propriety - inflammation is normally not transmural

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93
Q

histology findings in UC

A 
inflammatory infiltrate
goblet cell DEPLETION
glandular distortion
mucosal ulcers
CRYPT ABSCESSES
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94
Q

is smoking protective of uc

A

yes

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95
Q

symptoms of UC

A

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

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96
Q

signs of UC

A

acute, severe UC
- fever
tachycardia
tender, distended abdomen

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97
Q

extra-intestinal signs of uc

A 
erythema nodosum
episcleritis, scleritis
arthralgia
pyoderma gangrenosum
aphthous oral ulcers
PSC

sacroilitis
ankylosing spondylitis
amyloidosis

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98
Q

investigations for uc

A

BLOODS - FBC, U+E, ESR/CRP, LFT, Blood culture

stool mc&S - rule out infective cause

erect CXR - perforation

COLONOSCOPY + BIOPSY - DIAGNOSTIC

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99
Q

which scoring method used to assess UC severity

A

Truelove and Witt’s severity index

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100
Q

what parameters are found in truelove and witt’s index to diagnose uc

A 
number of motions in a day
rectal bleeding
temperature
resting HR
haemoglobin
ESR
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101
Q

complications of uc

A 
PERFORATION
HAEMORRHAGE
toxic megacolon
venous thrombosis 
colorectal cancer
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102
Q

first line recommended treatment for UC (proctitis + left sided colitis)

A

topical aminosalicylate (sulfasalazine)

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103
Q

second line rx for UC (proctitis) if no improvement after 4 weeks

A

add an oral aminosalicylate (mesalazine)

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104
Q

3rd line rx for UC (proctitis) if still no improvement

A

add a topical or oral corticosteroid for 4-8 weeks

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105
Q

second line rx for UC (left sided colitis) if no improvement after 4 weeks

A

add a high dose oral aminosalicylate

or

switch to a oral aminosalicylate + topical corticosteroid (4-8 weeks)

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106
Q

3rd line rx for UC (left sided colitis) if still no improvement

A

STOP TOPICAL TREATMENT

offer
- oral aminosalicylate +
oral corticosteroid (4-8 weeks)

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107
Q

first line rx for PANCOLITIS (UC)

A

topical aminosalicylate + oral aminosalicylate

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108
Q

2nd line rx for pancolitis after 4 weeks

A

STOP TOPICAL TREATMENT

offer
- oral aminosalicylate + oral corticosteroid (4-8 weeks)

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109
Q

rx for patients unsuitable for aminosalicylates in UC

A

give topical or an oral corticosteroid for 4-8 weeks

give oral corticosteroid in pancolitis

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110
Q

treatment of acute severe UC

A

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.

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111
Q

maintenance of remission in UC

A

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

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112
Q

what surgery required in UC

A

proctocolectomy + terminal ileostomy

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113
Q

what is crohn’s disease

A
  • 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
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114
Q

does smoking increase risk of crohn’s disease

A

yes - x3-4

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115
Q

symptoms of crohn’s disease

A

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

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116
Q

signs of crohn’s disease

A

aphthous oral ulcers
abdo tenderness
perianal abscess/fistulae/skin tags
anal strictures

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117
Q

complications of crohn’s disease

A 
small bowel obstruction
toxic megacolon
abscess 
fistulae 
perforation
haemorrhage 
small intestine cancer
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118
Q

investigation for crohn’s disease

A

bloods - FBC, U+E, ESR/CRP, LFT, B12, FOLATE, IRON PROFILE, CLOTTING

stool mc&s - exclude infection

COLONOSCOPY + BIOPSY

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119
Q

histology for crohns disease

A

transmural inflammation
non-caseating granulomas
goblet cells

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120
Q

non-pharmacological management of crohns disease

A

smoking cessation

optimise nutrition - elemental diet containing amino acids

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121
Q

rx - first presentation of crohns disease (Acute)

A

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)

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122
Q

maintenance therapy for crohns disease

A

azathioprine or mercaptopurine

2nd line - methotrexate

(DO NOT OFFER CORTICOSTEROIDS OR BUDOSENIDE)

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123
Q

maintenance of remission following surgery in crohns

A

azathioprine + metronidazole for 3 months

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124
Q

poor prognosis factors in crohns

A

onset at age <30y
steroids needed at first presentation.
perianal disease
diffuse small bowel disease

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125
Q

what is irritable bowel syndrome

A
  • 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
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126
Q

diagnosis of IBS

A

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
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127
Q

what criteria is required to diagnose IBS

A 
chronic symptoms (≥6 months)
exacerbated by stress, menstruation or gastroenteritis (post-infection IBS)
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128
Q

investigations for IBS

A

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

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129
Q

treatment for IBS

A
  • 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

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130
Q

what are risk factors for developing pancreatic cancer

A 
SMOKING
ALCOHOL
carcinogens
Diabetes
chronic pancreatitis
increased waist circumference
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131
Q

what type of carcinoma is pancreatic cancer

A

DUCTAL ADENOCARCINOMA

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132
Q

where is a common place for pancreatic cancer to arise

A

head of the pancreas

other

  • body
  • tail
  • ampulla of vater
  • pancreatic islet cells (insulinoma, gastrinoma)
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133
Q

which gene affected in pancreatic cancer

A

KRAS2 gene

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134
Q

typical presentation of pancreatic cancer

A

PAINLESS OBSTRUCTIVE JAUNDICE

other

  • anorexia
  • weight loss
  • diabetes
  • acute pancreatitis
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135
Q

signs of pancreatic cancer

A

JAUNDICE + PALPABLE GALLBLADDER (courvoisier’s law)

epigastric mass
hepatosplenomegaly
lymphadenopathy
ascites

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136
Q

investigations for pancreatic cancer

A

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.

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137
Q

treatment of pancreatic cancer

A

pancreato-duodenectomy (whipple’s procedure)

post-op chemo

palliation of jaundice - endoscopic or percutaneous stent insertion may help jaundice and anorexia.

pain - analgesia

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138
Q

which vitamin lacking in scurvy

A

vitamin C

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139
Q

signs of scurvy

A 
anorexia, cachexia
gingivitis, loose teeth, foul breath
bleeding from gums, nose, hair follicles or into joints, bladder, gut
muscle pain and weakness
oedema
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140
Q

treatment of scurvy

A

ascorbic acid

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141
Q

what is beriberi

A

lack of vitamin B1 (thiamine). wernickes causes this.

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142
Q

what is wet beriberi

A

heart failure with general oedema

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143
Q

what is dry beriberi

A

peripheral neuropathy

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144
Q

what is pallegra

A

lack of nicotinic acid.

classic triad - diarrhoea, dementia and dermatitis

  • ± neuropathy, depression, insomnia, tremor, rigidity, ataxia, fits
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145
Q

treatment of Allegra

A

o Education
o Electrolyte replacement
o Nicotinamide 100mg/4h PO

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146
Q

what is xerophthalmia

A

vitamin A deficiency syndrome

big cause of BLINDNESS IN THE TROPICS

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147
Q

what are carcinoid tumours

A

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).

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148
Q

common site for carcinoid tumour

A

appendix
ileum
rectum

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149
Q

what is carcinoid syndrome

A

occurs in 5% and implies hepatic involvement.

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150
Q

symptoms and signs of carcinoid syndrome

A

bronchoconstriction
paroxysmal flushing
diarrhoea
CCF

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151
Q

investigation for carcinoid syndrome

A

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
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152
Q

treatment of carcinoid syndrome

A

octreotide (somatostatin analogue)

tumour resection - only cure for carcinoid tumours.

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153
Q

what is a carcinoid crisis

A
  • 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)
154
Q

what are symptoms of malabsorption

A 
diarrhoea
weight loss
lethargy
steatorrhoea
bloating
155
Q

tests for malabsorption

A

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

156
Q

commonest causes of malabsorption in the UK

A

coeliac disease, chronic pancreatitis, crohn’s disease

157
Q

what is coeliac disease

A

T-cell mediated AUTOIMMUNE DISEASE OF THE SMALL BOWEL.

Gliadin intolerance causes villous atrophy and malabsorption.

158
Q

when is coeliac disease suspected

A

in those with diarrhoea + weight loss or ANAEMIA

159
Q

associations of coeliac disease

A

HLA-DQ2 (92%)
HLA-DQ8
autoimmune disease

DERMATITIS HERPETIFORMIS

160
Q

presentation of coeliac disease

A 
steatorrhoea/smelly stools
diarrhoea
abdo pain
bloating
nausea and vomiting

weight loss
fatigue
weakness

1/3 asymptomatic

161
Q

signs of coeliac disease

A

aphthous oral ulcers
angular stomatitis

osteomalacia
failure to thrive in children

162
Q

investigations for coeliac disease

A

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

163
Q

treatment for coeliac disease

A

lifelong gluten free diet

rice maize soya potatoes oats and sugar are ok.

164
Q

complications of coeliac disease

A 
ANAEMIA
2° lactose intolerance
GI T-cell lymphoma (rare)
INCREASED RISK OF MALIGNANCY (gastric, oesophageal, bladder, breast, brain)
myopathies
neuropathies
hyposplenism
osteoporosis
165
Q

symptoms of chronic pancreatitis

A

epigastric pain radiates to back
relieved by sitting forward

bloating
steatorrhoea
weight loss
brittle diabetes

166
Q

causes of chronic pancreatitis

A 
ALCOHOL
CF
haemochromatosis
pancreatic duct obstruction
high PTH
congenital
167
Q

investigations for chronic pancreatitis

A

ultrasound ± CT (pancreatic calcification)

AXR - speckled calcification

168
Q

treatment of chronic pancreatitis

A

analgesia
lipase
fat-soluble vitamins
insulin - variable

surgery for unremitting pain, narcotic abuse, weight loss- pancreatectomy or pancreaticojejunostomy

169
Q

complications of chronic pancreatitis

A 
pseudocyst
diabetes
biliary obstruction
local arterial aneurysm
splenic vein thrombosis
gastric varices
pancreatic carcinoma
170
Q

tools used to assess alcohol dependence

A

CAGE questionnaire

AUDIT

171
Q

Alcoholic hepatitis - what are the raised parameters on bloods

A 
AST:ALT >2
high GGT
high MCV
high INR
high urea
high WCC

low platelets - hypersplenism or toxicity

172
Q

signs of severe alcoholic hepatitis

A

jaundice
encephalopathy
coagulopathy

173
Q

treatment of alcoholic hepatitis

A

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.

174
Q

what is found on histology for cirrhosis (biopsy findings)

A

mallory bodies

neutrophil infiltrate

175
Q

CNS signs of alcohol excess

A

wernicke’s encephalopathy
korsakoff’s - confabulation

cortical atrophy
retrobulbar neuropathy
seizures
falls
wide-based gait
neuropathy
176
Q

GI signs of alcohol excess

A 
obesity
d+v
gastric erosions
peptic ulcers
varices
pancreatitis
cancer - oesophagus, stomach, pancreatic, mouth, liver
oesophageal rupture (Boerhaave's syndrome - shock and surgical emphysema)
177
Q

alcohol excess findings on bloods

A

high MCV, anaemia - megaloblastic anaemia due to bone marrow depression, GI bleeding, alcoholism-related folate deficiency, haemolysis, sideroblastic anaemia.

178
Q

heart problems in alcoholics

A

arrhythmia
high BP
cardiomyopathy
sudden death

179
Q

symptoms of alcohol withdrawal and time frame

A

starts 10-72h after last drink

  • tachycardia
  • hypotension
  • tremor
  • confusion
  • seizures
  • delirium tremens - hallucinations (animals crawling over skin)
180
Q

pregnancy complication of alcohol excess

A

fetal alcohol syndrome - low iq, short palpebral fissure, absent philtrum, small eyes

181
Q

management of alcohol withdrawal

A

admit, do BP
chlordiazepoxide (wean over 7-10d).
alternative - diazepam

182
Q

long term treatment of alcohol withdrawal to prevent relapse

A

disulfiram

acamprosate

group therapy - AA

183
Q

5 causes of abdominal distention

A 
flatus - obstruction
faeces - stool impaction
fetus - pregnancy
fluid - ascites
fat - obesity
184
Q

if ascites suspected, how to investigate

A

aspirate ascitic fluid (paracentesis) - cytology, culture and protein level (≥30g/l)

ultrasound abdomen

185
Q

causes of ascites

A 
malignancy
infection - tb
low albumin
CCF
pancreatitis
myxedema
186
Q

causes of ascites with portal hypertension

A

cirrhosis
budd-chiari syndrome
ivc or portal vein thrombosis
portal nodes

187
Q

causes of splenomegaly with fever

A

infection - malaria, SBE/IE, hepatitis, EBV, CMV, TB, HIV

sarcoid
malignancy

188
Q

splenomegaly with arthritis causes

A 
sjogrens syndrome
RA
SLE
infection - lyme disease
vasculitis/behcets
189
Q

splenomegaly with anaemia

A 
sickle cell disease
thalassaemia
leishmaniasis
leukaemia
pernicious anaemia
190
Q

splenomegaly with lymphadenoapthy

A

glandular fever
leukaemia
lymphoma
sjogrens

191
Q

splenomegaly with ascites

A

carcinoma

portal hypertension

192
Q

splenomegaly with weight loss + CNS signs

A

cancer
lymphoma
TB

193
Q

splenomegaly with purpura

A

septicaemia
DIC
meningococcaemia

194
Q

splenomegaly with murmur

A

SBE/IE

rheumatic fever

195
Q

massive splenomegaly causes

A 
malaria
myelofibrosis
CML
gaucher's syndrome
leishmaniasis
196
Q

acute abdomen - clinical syndromes requiring laparotomy

A

rupture of organ - spleen, aorta, ectopic pregnancy

shock is the leading sign

abdo swelling

hx of trauma: blunt trauma = spleen, penetrating trauma -= liver

PERITONITIS

197
Q

what is peritonitis

A

perforation of peptic ulcer/duodenal ulcer, diverticulum, appendix, bowel or gallbladder

198
Q

signs of peritonitis

A 
shock
lying still
tenderness 
rebound tenderness
board-like abdominal rigidity
guarding
no bowel sounds
199
Q

investigation for peritonitis

A

ERECT CXR - pneumoperitoneum

200
Q

signs of abscess

A

swelling
swinging fever
high WCC

201
Q

what is colic

A

regular waxing and waning pain

caused by muscular spasm in a hollow viscus - gut, ureter, sapling, uterus, bile duct or gallbladder

restlessness

202
Q

investigation for peritonitis

A

bloods - abc, u&e, AMYLASE, LFT, CRP, ABG (?mesenteric ischaemia), urinalysis

203
Q

imaging for peritonitis

A

erect CXR

AXR - may show Rigler’s sign

USS - may identify perforation or free fluid immediately

204
Q

treatment of peritonitis

A 
NBM
treat shock
crossmatch/ group and save
blood cultures
antibiotics - cefuroxime + metronidazole

analgesia
iv fluids

ECG if >50y ?AAA

205
Q

causes of a medical acute abdomen

A 
IBS 
MI
mesenteric ischaemia
acute pancreatitis
leaking AAA
gastroenteritis
lower lobe pneumonia
thyroid storm
TB
sickle cell crisis
phaeochromocytoma
206
Q

symptoms of acute appendicitis

A

periumbilical pain that moves to the RIF

pain precedes vomiting in surgical abodmen

207
Q

general signs of acute appedicitis

A 
tachycardia
fever (low grade) 37.5-38.5
furred tongue
lying still
foetor ± flushing
shallow breaths
coughing hurts
208
Q

signs of acute appendicitis

A

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

209
Q

investigation for acute appendicitis

A

bloods - neutrophil leukocytosis, elevated CRP

if female - DO A PREGNANCY TEST

ABDO USS

CT abdo pelvis more accurate but can cause fatal delay

210
Q

treatment of acute appendicitis

A

prompt appendicectomy
antibiotics - cefuroxime + metronidazole

laparoscopy - done in women and obese

211
Q

complications of acute appendicitis

A

perforation
appendix mass
appendix abscess

212
Q

division points of the foregut

A

proximal to 2nd part of duodenum

supplied by coeliac trunk

213
Q

midgut division points

A

2nd part of duodenum to 2/3 along transverse colon

supplied by SMA

214
Q

hindgut division points

A

1/3 along transverse colon to anus

supplied by IMA

215
Q

pathology of pain in acute appendicitis

A

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)

216
Q

differential diagnosis of RIF pain

A 
ectopic pregnancy
UTI
mesenteric adenitis
cholecystitis
diverticulitis
PID
crohns disease
perforated ulcer
PID
217
Q

bowel obstruction features

A

nausea and vomiting
colicky abdominal pain
constipation (absolute - no flatus passed)
abdominal distention

fever
tachy

faeculent vomiting - late sign (colonic fistula with proximal gut)

218
Q

causes of obstruction (mechanical)

A

Adhesions - commonest cause in SBO

colorectal cancer

intussusception - common in children (ileocaecal valve)

hernia

volvulus- caecum and volvulus

219
Q

causes of obstruction (pseudo-obstruction)

A

paralytic ileus - post-op likely, pancreatitis, spinal injury, low K, low Na, uraemia, peritoneal sepsis and drugs

neuropathy

hirschsprung disease

220
Q

AXR findings in SBO

A

central gas shadows with valvulae conniventes spanning across the lumen

221
Q

AXR in LBO

A

peripheral gas shadows proximal to the blockage (caecum)

large bowel haustra do not cross the lumen’s width

222
Q

common causes of SBO

A

adhesions

hernia

223
Q

common causes of LBO

A

malignancy
diverticular disease
volvulus

224
Q

complications of bowel obstruction

A

bowel ischaemia
perforation
sepsis

225
Q

management of bowel obstruction

A

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

226
Q

characteristic sign of sigmoid volvulus on AXR

A

‘coffee bean’ sign

inverted ‘u’ loop of bowel

227
Q

management of sigmoid volvulus

A

sigmoidoscopy + insertion of a FLATUS TUBE

228
Q

classic triad of stomach volvulus causing obstruction

A

vomiting
pain
failed attempts to pass NG tube

229
Q

complications of gastric volvulus

A

incarceration

strangulation

230
Q

risk factors for gastric volvulus

A

congenital

  • paraoesophageal hernia
  • congenital bands
  • bowel malformations
  • pyloric stenosis

acquired
- gastric/oesophageal surgery

231
Q

investigations for gastric volvulus

A

erect CXR - gastric dilatation and double fluid level

232
Q

treatment of gastric volvulus

A

acutely unwell - prompt resus and laparotomy

233
Q

definition of a hernia

A

protrusion of a viscus or part of a viscus through a defect of the walls of its containing cavity into an abnormal position.

234
Q

what is a irreducible hernia

A

Said to be irreducible if they cannot be pushed back into the right place.

235
Q

what is a incarcerated hernia

A

contents of the hernial sac stuck inside by adhesions

236
Q

what is an obstructed hernia

A

gastrointestinal hernias are obstructed if bowel contents cannot pass through them - the classical features of intestinal obstruction occur.

237
Q

what is a strangulated hernia

A

if ischaemia occurs, the patient becomes toxic and requires urgent surgery.

238
Q

femoral hernia - what is it

A

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.

239
Q

who does a femoral hernia commonly affect

A

middle aged women and the elderly

240
Q

anatomical location of femoral hernias

A

inferior and lateral to the pubic tubercle

241
Q

treatment of femoral hernia

A

surgical repair
herniotomy - ligation and excision of sac
herniorrhaphy - repair of the hernial sac

242
Q

what is gastroschisis

A

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

243
Q

what is an exomphalos (omphalocele)

A

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.

244
Q

what is a direct inguinal hernia

A

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

245
Q

what is indirect inguinal hernia

A

push through the deep internal ring, and if large, out through the external ring.

lateral to the inferior epigastric vessels

246
Q

which conditions predispose to umbilical hernia

A 
MALES > FEMALES
chronic cough
constipation
urinary obstruction
heavy lifting
ascites
past abdominal surgery (e.g. damage to the iliohypogastric nerve during appendicectomy)
247
Q

where is the deep ring found

A

mid-point of the inguinal ligament

248
Q

where is the superficial ring found

A

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)

249
Q

relations of the inguinal canal

A
  • 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
250
Q

examination of a lump in the groin

A
  • 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
251
Q

how to distinguish between direct and indirect hernias

A

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
252
Q

treatment of inguinal hernias

A

weight loss
smoking cessation

laparoscopic repairs
- transabdominal pre-peritoneal (TAPP)

  • totally extraperitoneal (TEP)
253
Q

when is return to work advised for patients with inguinal hernias

A

advise 4 weeks rest and convalescence over 10 weeks

254
Q

what are the contents of the inguinal canal in a male

A
  • 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
255
Q

what are the contents of the inguinal canal in a female

A

the round ligament of the uterus

256
Q

what type of cancer is a colorectal cancer

A

adenocarcinoma

affects >60 year olds

257
Q

predisposing factors to colorectal cancer

A 
neoplastic polyps
IBD
genetic - FAP + HNPCC
diet - low fibre, increased red and processed meats
excessive alcohol
smoking
previous cancer
258
Q

how to prevent colorectal cancer

A

aspirin - thought to inhibit polyp growth

259
Q

presenting features of colorectal cancer- left-sided

A

bleeding/mucus PR
altered bowel habit or obstruction
tenesmus
mass PR

weight loss
fever, night sweats

perforation
haemorrhage
fistula

260
Q

presenting features of colorectal cancer- right-sided

A

weight loss
low Hb
abdominal pain
obstruction less likely

261
Q

investigations for colorectal cancer

A

FBC - microcytic anaemia
faecal immunochemical test (FIT)

COLONOSCOPY + BIOPSY

CT/MRI

CEA - used to monitor disease and effectiveness of treatment

262
Q

dukes staging for colorectal cancer

A

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%

263
Q

treatment of colorectal cancer

A

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.

264
Q

is there screening available to detect colorectal cancer

A

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.

265
Q

what are different types of polyps found in the bowel

A
  1. INFLAMMATORY
    o UC, crohns, lymphoid hyperplasia
  2. HAMARTOMATOUS
    o Juvenile polyps
    o Peutz-Jeghers
  3. 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
266
Q

what type of cancer is a stomach cancer

A

adenocarcinomas

267
Q

presentation of stomach cancer

A

non-specific

dyspepsia
weight loss
vomiting
dysphagia
anaemia
268
Q

signs of stomach cancer

A

large left supraclavicular (Virchow’s node) = Troisier’s sign

acanthosis nigricans

epigastric mass
hepatomegaly
jaundice
ascites

269
Q

investigation for stomach cancer

A

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
270
Q

treatment for stomach cancer

A

partial gastrectomy - may suffice for distal tumours

total gastrectomy - more proximal tumours

adjuvant chemotherapy

271
Q

risk factors for developing oesophagus cancer

A 
ALCOHOL excess
smoking
diet
achalasia
plummer-vinson syndrome
obesity
reflux oesophagitis
± barrett's oesophagus
272
Q

which type of cancer affects the distal oesophagus

A

ADENOCARCINOMA

273
Q

which type of cancer affects the proximal oesophagus

A

SQUAMOUS CELL CARCINOMA

274
Q

presentation of oesophagus cancer

A

dysphagia
dysphonia (hoarse voice)
dyspnoea (airway obstruction)

weight loss
retrosternal chest pain

275
Q

investigation for oesophagus cancer

A

OGD with biopsy

276
Q

staging for oesophagus cancer

A
  • 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
277
Q

management of oesophagus cancer

A

if localised T1/T2 - radical curative oesophagectomy

278
Q

cause of oesophageal rupture

A

iatrogenic - endoscopy/biopsy/dilatation (85-90%)
trauma - penetrating injury/ingestion of foreign body
carcinoma
boerhaave syndrome - rupture due to violent vomiting
corrosive ingestion

279
Q

clinical features of oesophageal rupture

A

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.

280
Q

treatment of oesophageal rupture

A

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.

281
Q

what is a major risk factor for a cholangiocarcinoma

A

PSC

282
Q

management of cholangiocarcinoma

A

surgical resection

if palliative - biliary stenting and chemotherapy

283
Q

what must you consider in a patient presenting with abdominal pain who has AF

A

mesenteric ischaemia

284
Q

what is acute mesenteric ischaemia

A

Almost always involves the SMALL BOWEL and may follow SMA THROMBOSIS OR EMBOLISM, MESENTERIC VEIN THROMBOSIS, OR NON-OCCLUSIVE DISEASE.

285
Q

what is the cause of acute mesenteric ischaemia

A

Arterial thrombus or an embolic event would cause it

286
Q

presenting symptoms of acute mesenteric ischaemia

A

acute severe abdominal pain
no abdominal signs
rapid hypovolaemia –> shock

287
Q

investigations for acute mesenteric ischaemia

A 
high lactate
high WCC
persistent metabolic acidosis
high Hb 
modestly raised plasma amylase
288
Q

imaging for acute mesenteric ischaemia

A

CT/MRI angiography
arteriography
ECG

289
Q

treatment of acute mesenteric ischaemia

A 
ABCDE
resuscitation with
- IV fluids
- IV Abx (gentamicin + metronidazole)
- LMWH

surgery - remove necrotic bowel (laparotomy)

ITU

290
Q

what is chronic mesenteric ischaemia

A

‘Intestinal angina’

291
Q

triad of chronic mesenteric ischaemia

A

severe, colicky post-prandial abdominal pain (‘gut claudication’)

weight loss

upper abdominal bruit

+PR bleeding, malabsorption, n+v

292
Q

cause of chronic mesenteric ischaemia

A

vascular disease (95% due to diffuse atherosclerotic disease in all 3 mesenteric arteries)

293
Q

investigations for chronic mesenteric ischaemia

A

CT angiography and contrast enhanced MR angiography

doppler USS

294
Q

treatment for chronic mesenteric ischaemia

A

surgery considered - risk of ongoing risk of acute infarction.

295
Q

what is ischaemic colitis

A

low flow in the inferior mesenteric artery territory

ranges from mild ischaemia to gangrenous colitis

296
Q

presentation of ischaemic colitis

A

lower left-sided abdo pain

bloody diarrhoea

297
Q

investigation for ischaemic colitis

A

colonoscopy + biopsy - gold standard

barium enema - shows characteristic ‘thumb’ printing of submucosal swelling

298
Q

treatment for ischaemic colitis

A

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.

299
Q

what are the physical complications of gastrectomy and peptic ulcer surgery

A

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

300
Q

metabolic complications of gastric surgery

A

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

301
Q

complications of peptic ulcer disease

A

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)

302
Q

what is severe obesity associated with

A 
T2DM
hypertension
IHD
sleep apnoea
osteoarthritis
depression
303
Q

indications for bariatric surgery

A

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.

304
Q

what are the 2 main mechanisms by which bariatric surgery help reduce weight

A
  • restriction of calorie intake by reducing stomach capacity.
  • malabsorption of nutrients by reducing the length of functioning small bowel
305
Q

2 main procedures in bariatric surgery

A

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.

306
Q

presentation of pyloric stenosis in child

A

first 3-8 weeks
projectile vomiting
M:F 4:1

baby is malnourished and always hungry

307
Q

investigation for pyloric stenosis

A

ultrasound abdomen - hypertrophied pylorus muscle

308
Q

examination findings of pyloric stenosis

A

palpate the olive-shaped pyloric mass in the RUQ during feed.

visible gastric peristalsis starts in the LUQ

309
Q

cardinal electrolyte + ABG finding in pyloric stenosis

A

hypocholaraemic, hypokalaemic metabolic alkalosis

310
Q

treatment for pyloric stensosi

A

ramstedt’s pyloromyotomy

311
Q

presentation of intussusception in paediatrics

A

typical age - 5-12months
episodic intermittent inconsolable crying.

drawing up of legs (colic)
billous vomiting
REDCURRANT STOOLS (blood PR)

312
Q

diagnosis of intussusception

A

sausage shaped mass on palpation

may become shocked

USS abdomen - target sign

313
Q

management of intussusception

A

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

314
Q

presentation of midgut rotation in paediatrics

A

dark green bilious vomiting
distention
rectal bleeding

315
Q

imaging for malrotation in children

A

upper GI contrast study - barium swallow

316
Q

treatment of malrotation in children

A

resuscitation

surgery - broadening mesentery and untwisting bowel

317
Q

what are diverticula

A

a GI diverticulum is an out pouching of the gut wall, usually at sites of entry of perforating arteries.

318
Q

what are the 3 types of diverticular disease

A

Diverticulosis – diverticula are present

Diverticular disease – implies that the diverticula are symptomatic

Diverticulitis – inflammation of a diverticulum

319
Q

where is the most common site for diverticulae

A

sigmoid colon

320
Q

underlying pathology of diverticular disease

A

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.

321
Q

presenting features of diverticular disease

A

altered bowel habit ± left-sided colic relieved by defecation.

nausea

flatulence

322
Q

features of diverticulitis

A

altered bowel habit
nausea
flatulence

pyrexia
high WCC
high CRP/ESR
tender colon
± localised or generalised peritoneum
323
Q

diagnosis of diverticular disease

A

CT ABDOMEN - gold standard to confirm acute diverticulitis.

ERECT CXR - ?perforation

DONT DO COLONOSCOPY ACUTELY - RISK PERFORATION

324
Q

treatment of diverticulitis

A 
analgesia
NBM
IV fluids
antibiotics
CT-guided percutaneous drainage if abscess
325
Q

complications of diverticulitis

A 
perforation
haemorrhage
fistulae - enterocoelic, colovaginal, colovesicle
abscess
post-infective strictures
326
Q

management of haemorrhage - diverticulitis

A

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

327
Q

what is angiodysplasia

A

submucosal arteriovenous malformations

typically present as FRESH PR BLEEDING IN ELDERLY.

328
Q

pathology of angiodysplasia

A

70-90% lesions occur in right colon, though angiodysplasia can affect anywhere in GI tract.

329
Q

diagnosis of angiodysplasia

A

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

330
Q

treatment of angiodysplasia

A

embolisation

endoscopic laser electrocoagulation

resection

331
Q

causes of rectal bleeding

A 
diverticulitis
colorectal cancer
haemorrhoids
IBD
perianal disease
angiodysplasia
ischaemic colitis
332
Q

perianal disease - pruritus ani causes

A

itch occurs if the anus is moist/soiled; fissures, incompetence, poor hygiene, tight pants, threadworm, fistula, dermatoses, lichen sclerosis, anxiety, contact dermatitis.

333
Q

treatment of pruritus ani

A 
careful hygiene
anaesthetic cream
moist-wipe post defecation
no spicy food
no steroid/antibiotic cream
capsaicin may help
334
Q

what are the causes of fissure-in-ano

A

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.

335
Q

rare causes of fissures

A 
syphilis
herpes
trauma
crohns
anal cancer
psoriasis
336
Q

treatment of fissures

A

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

337
Q

what is a fistula-in-ano

A

track communicates between the skin and anal canal/rectum

338
Q

pathophysiology of fistula-in-ano

A

blockage of deep intramuscular gland ducts is thought to predispose to the formation of abscesses which discharge to form the fistulae

339
Q

causes of fistula-in-ano

A 
perianal sepsis
abscesses
crohn's disease
TB
diverticular disease
rectal carcinoma
immunocompromise
340
Q

investigation for fistula-in-ano

A

MRI

endoanal US scan

341
Q

treatment of fistula-in-ano

A

fistulotomy + excision

342
Q

where are anorectal abscesses most likely and rx

A

perianal (45%)

ischiorectal (30%)
intersphincteric (20%)
supralevator (5%)

rx - incise and drain under GA

343
Q

causes of anorectal abscesses

A

DM
crohn’s
malignancy
fistulae

344
Q

what is a pilonidal sinus

A

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.

345
Q

who is a pilonidal sinus more common in

A

males
obese caucasians
asia, middle east and mediterranean at high risk

346
Q

treatment of a pilonidal sinus

A

excision of sinus tract ± primary closure.

offer hygiene and hair removal advice

347
Q

causes of rectal prolapse

A

lax sphincter
prolonged straining
related to chronic neurological and psychological disorders.

348
Q

treatment of rectal prolapse

A

fix rectum to sacrum (rectopexy) ± mesh insertion ± rectosigmoidectomy

349
Q

treatment of perianal warts (condylomata acuminata)

A

podophyllotoxin or imiquimod
OR
cryotherapy/surgical excision

350
Q

what is proctalgia fugax and treatment

A

idiopathic, intense, brief, stabbing/crampy rectal pain.

worse at night.

rx - reassurance. inhaled salbutamol or topical GTN or topical diltiazem may help

351
Q

what type of cancer is an anal cancer

A

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.

352
Q

risk factors for anal cancer

A

HPV 16, 6, 11, 18, 31, 33
syphilis
anoreceptive homosexuals

353
Q

presentation of anal cancer

A 
bleeding
pain
bowel habit change
pruritus ani
masses
stricture
354
Q

treatment of anal cancer

A

chemo-irradiation (inc radiotherapy)

355
Q

what are haemorrhoids

A

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.
356
Q

why do internal haemorrhoids not cause pain

A

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

357
Q

causes of haemorrhoids

A

constipation with prolonged straining.

congestion from a pelvic tumour
pregnancy
CCF
portal hypertension

358
Q

classification of haemorrhoids

A

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

359
Q

symptoms of haemorrhoids

A

bright red rectal bleeding
mucuous discharge
pruritus ani

severe anaemia may occur
no pain usually unless thrombosed.

360
Q

investigation for haemorrhoids

A

PR EXAM
abdominal examination

proctoscopy - internal haemorrhoids

361
Q

treatment for haemorrhoids

A

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
362
Q

management of prolapsed, thrombosed piles

A

treat with analgesia, ice packs, and stool softeners.

363
Q

what is bile composed of

A

cholesterol
bile pigments
phospholipids

364
Q

what is a pigmented gallstone

A

small, friable and irregular

cause is haemolysis

365
Q

what is a cholesterol gallstone

A 
large, often solitary
causes
- male
- age
- obesity
366
Q

what is a mixed gallstone

A

calcium stones, pigment and cholesterol

367
Q

what is acute cholecystitis

A

inflammation of the gallbladder - may cause continuous epigastric or RUQ pain (referred to right shoulder), vomiting, fever, local peritonism, or a gallbladder mass.

368
Q

common sign in acute cholecystitis

A

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

369
Q

tests for acute cholecystitis

A
  • High WCC
  • ULTRASOUND
    o Thick-walled, shrunken GB, pericholecystic fluid, stones, CBD (dilated if >6mm)
370
Q

treatment for acute cholecystitis

A

NBM
analgesia
IV fluids
antibiotics e.g. cefuroxime

<1 week - laparoscopic cholecystectomy

371
Q

complications of gallstones

A 
-	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
372
Q

what is acute pancreatitis

A

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
373
Q

causes of acute pancreatitis

A
  • Gallstones
  • Ethanol (alcohol)
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune (PAN)
  • Scorpion venom
  • Hyperlipidaemia, hypothermia, hypercalcaemia
  • ERCP and emboli
  • Drugs
374
Q

symptoms of acute pancreatitis

A
  • Gradual or sudden severe epigastric or central abdominal pain (radiates to back, sitting forward may relieve)
  • VOMITING
375
Q

signs of acute pancreatitis

A
  • 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.
376
Q

tests for acute pancreatitis

A

serum amylase
serum lipase
ABG
erect CXR

USS - screening for gallstones

CT abdomen - standard choice of imaging

377
Q

score used to assess severity of acute pancreatitis

A

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
378
Q

treatment of acute pancreatitis

A 
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
379
Q

early complications of acute pancreatitis

A 
shock
ARDS
renal failure
DIC
sepsis
low calcium
high glucose
380
Q

late complications of acute pancreatitis

A 
pancreatic necrosis 
pseudocyst
abscess
bleeding 
thrombosis
fistulae
recurrent oedematous pancreatitis

Finals (4 decks)

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