General surgery, Gastro and hepatology Flashcards
Appendicitis
acute inflammation of the vermiform appendix usually due to obstruction of the appendiceal lumen
Epidemiology of appendicitis
Most common cause of acute abdomen in children & adults
usually presents age 10-20yrs
Most common cause of acute abdomen
Appendicitis
Presentation of appendicitis
Abdominal pain (usually severe)
- starts periumbilical then migrates to RIF due to peritoneal inflammation
- worse on movement/coughing (i.e. pt lies still)
Nausea & vomiting
mild pyrexia
guarding, rebound tenderness, tenderness
Rovsing’s sign +ve: palpation of LIF leads to pain in RIF
Psoas sign +ve in retrocaecal appendix: pain on hip extension
Investigations for appendicitis
essentially a clinical diagnosis
FBC (↑ WCC, neutrophilia)
Pregnancy tests in females
CRP (↑)
USS or CT ± contrast
Management of appendicitis
appendectomy
-laparoscopic = 1st line
prophylactic Abx
analgesia
Complications of appendicitis
perforation (~20%) appendix abscess (after untreated perforation)
Aetiology of acute pancreatitis
GET SMASHED
G: gallstones
E: ethanol
T: trauma
S: steroids M: mumps A: autoimmune S: scorpion stings H: hypercalcaemia E: ERCP D: drugs e.g. mesalazine
Most common causes of acute pancreatitis
biliary pancreatitis (i.e. after gallstones)
alcohol induced
post ERCP, steroids, trauma
Presentation of acute pancreatitis
constant severe epigastric pain radiating to back -worse after meals -better when leaning forward N&V jaundice shock (hypotension, tachycardia) dyspnoea
Investigations for acute pancreatitis
often a clinical diagnosis
serum amylase (↑, often >3x upper limit of normal)
serum lipase (↑, often >3x upper limit of normal)
FBC (↑WCC)
U&Es
CRP
plain erect AXR
Glasgow score use
used for acute pancreatitis as a prognostic tool
alternatives include the RANSON score and the APACHE II score
Glasgow score for acute pancreatitis
Age >55 yrs WCC >15x10^9/L Urea >16 mmol/L glucose >10 mmol/L pO2 <8 kPa albumin <32 g/L Ca2+ <2 mmol/L LDH >600 units AST/ALT >200 units
Poor prognostic indicators for acute pancreatitis
age > 55 years hypocalcaemia hyperglycaemia hypoxia neutrophilia elevated LDH and AST
Management of acute pancreatitis
aggressive IV fluid therapy Nil by mouth NG tube feeding analgesia consider Abx if severe Early cholecystectomy/ERCP if related to gallstones
Chronic pancreatitis
caused by progressive inflammation & irreversible damage to the structure and exocrine/endocrine functions of the pancreas
Aetiology of chronic pancreatitis
~80% due to long term heavy chronic alcohol misuse
others: cystic fibrosis, heamachromatosis, ductal obstruction
Epidemiology of chronic pancreatitis
average pt is aged 40 yrs
4:1 male: female ratio
Presentation of chronic pancreatitis
epigastric pain -radiates to back -worse after meals (i.e. exacerbated by eating) -begins episodic then becomes constant weight loss pancreatic diabetes steatorrhoea -cramping/bloating Vit ADEK deficiency secondary to steatorrhoea
Investigations for chronic pancreatitis
AXR (pancreatic calcification)
CT (more sensitive for calcifications)
FBCs/U&Es/creatinine/LFTs/Ca2+/glucose
amylase (is normal)
Management of chronic pancreatitis
analgesia (often requires opioids) pancreatic enzyme replacement e.g. CREON abstinence from alcohol/smoking/drugs supplements such as Vit ADEK surgery if intractable pain
Diverticular disease
a set of colonic pathologies resulting from the abnormal out pouching of the colonic mucosa i.e. diverticula
Includes:
Diverticulosis (non-inflamed diverticuli)
Diverticulitis (inflammed/infected diverticuli)
Aetiology of diverticular disease
develop due to chronic elevations of intraluminal pressure e.g. due to constipation & the age related weakening of connective tissue
Risk factors diverticular disease
age >50 yrs
low fibre diet
obesity
Presentation of Diverticulosis
non specific abdo pain/discomfort
chronic constipation
bloating
Presentation of Diverticulitis
LLQ pain (NB pts of asian pts tend to have right sided diverticuli so present with LRQ pain) altered bowel habit (diarrhoea/constipation) localised tenderness on palpation
Presentation of diverticular haemorrhage
painless abrupt frank PR bleeding
Investigations for diverticular disease
if asymptomatic its usually and incidental finding
colonoscopy (diagnostic modality of choice) FBCs (↑ WCC)/CRP (↑) in diverticulitis U&Es barium enema CT cologram
Management of diverticular disease
↑ dietary fibre intake & ensure adequate fluid intake
analgesia
ABx for diverticulitis
surgery if perforation/uncontrolled sepsis/fistula
Complications of diverticular disease
fistulas perforation leading to peritonitis abscess formation haemorrhage intestinal obstruction
Hepatitis A (Hep A)
a viral hepatitis that is not associated with chronic liver disease
Key facts: most common form of acute viral hepatitis NOTIFIABLE disease in UK DOES NOT CAUSE CHRONIC DISEASE transmitted faeco-oral route
Hep A risk factors
travel to high risk areas e.g. tropics, male homosexuality + multiple partners, IVDU, personal contacts, pts with clotting disorders receiving factor VIII & IX
Presentation of Hep A
Flu like prodrome (fevers, malaise, myalgia)
RUQ pain
tender hepatomegaly
jaundice ± pruritus/pale stools/dark urine
Specific investigations for Hep A
anti-HAV IgG (↑)
-persist indefinitely=sign of previous infection/vaccination
anti-HAV IgM (↑)
-present in active infection
HAV RNA (+ve)
Investigations for acute viral hepatitis
ALT ↑ AST ↑ ALP ↑ gamma-GT ↑ bilirubin ↑
Management of Hep A
supportive management
avoid alcohol
avoid food handling
avoid unprotected intercourse
Hep A vaccination
not routinely given
consider if high risk pt e.g. MSM, IVDU, sewage workers, pts with chronic liver disease, pts with haemophilia
Hepatitis B (Hep B)
most common cause of hepatitis world wide
transmitted sexually, parenterally or perinatally
Acute presentation of Hep B
acute illness often sub clinical or presents as flu like illness (similar to Hep A)
Chronic presentation of Hep B
chronic disease (if HbsAg +ve for >6 months) fatigue, RUQ pain
Hep B investigations
LFTs (ALP/AST/ALT/bilirubin ↑)
HBsAg (+ve in acute disease)
HbeAg (+ve implies infectivity, i.e. recent infection)
HbcAg i.e. anti-HBc (+ve implies past infection, if only vaccinated -ve)
HbsAg i.e. anti-HBs (+ve if vaccinated or immunity)
Prevention of Hep B
vaccination
on routine childhood immunisation schedule
given at 2,3 and 4 months
Complications of Hep B
↑ risk of hepatocellular carcinoma (HCC)
chronic hepatitis
Hepatits C (Hep C)
transmitted parenterally e.g. IVDU/needlestick
↑ cases in UK
Presentation of Hep C
~80% initially asymptomatic initially, ~20% acute hepatitis (malaise, RUQ pain, tender hepatomegaly, jaundice)
Chronic infection (>6 months HCV RNA +ve) liver cirrhosis, arthralgia/arthritis, HCC, cryoglobulinaemia, membranoproliferazive glomerulonephritis
Investigations for Hep C
LFTs (↑ AST/ALT/ALP/GGT/bilirubin)
Hep C antibodies (+ve in immunocompetent pts)
HCV RNA (+ve)
Treatment for Hep C
Acute:
active monitoring or interferon to ↓ risk of chronic HCV
Chronic:
combination of protease inhibitors ± ribavirin
Viral hepatitis unable to vaccinated against
Hep C has no vaccine currently available
Hepatitis D (Hep D)
Virus requiring Hep B surface antigen to survive, so only develops in pts with HBsAg
i.e. as co-infection or superinfection with HBV
treated with interferon
Cirrhosis
a process characterised by diffuse fibrosis & conversion of normal liver architecture to structurally abnormal nodules known as regenerative nodules
the final stage of a variety of liver diseases
Aetiology of cirrhosis
Alcoholic liver disease
Hep B & Hep C infections
Non alcoholic fatty liver disease (NAFLD)
Others: haemochromatosis, primary biliary cirrhosis, primary sclerosis cholangitis
Risk factors for liver cirrhosis
excess alcohol consumption Hep B/C infection obesity IVDU unprotected sexual intercourse
Presentation of cirrhosis
often asymptomatic until decompensation
symptoms are generally vague
oedema, ascites, easy bruising, pruritus, jaundice, spider naevi, palamar erythema, leuchonychia, hepatomegaly,, nodular liver
Investigations for cirrhosis
LFTs -AST ↑ -ALT ↑ -GGT ↑ -ALP ↑ albumin ↓ FBC (↓Hb, thrombocytopenia) coagulation screen (↑ prothrombin time) transient elastography/acoustic radiation impulse imaging
Hep B/C serology, U&Es, ceruplasmin, urinary copper, ferritin, haemateninics
NB if AST > ALT indicates alcoholic liver disease, but ALT > AST suggests other causes
Classification of cirrhosis
Child-Pugh-Turcotte system
Management of cirrhosis
treat underlying cause
ensure adequate nutrition
stop alcohol intake
Zinc supplements (Zinc deficiency common)
Hep A/influenza/pneumococcal vaccinations
liver transplant (only curative measure)
Compensated vs decompensated cirrhosis
compensated = liver still able to function, generally minimal symptoms present
decompensated = liver not properly functioning leading to features such as jaundice, ascites etc
oesophageal varices
occur at the junction of the portal & systemic venous circulation usually in the distal oesophagus and/or proximal stomach
due to portal hypertension leading to dilation of the anastomosis of the 2 venous systems
Presentation of oesophageal varices
generally asymptomatic unless haemorrhaging haematemesis abdo pain malaena dysphagia/odynophagia pallor shock (hypotension, tachycardia, ↓ GCS)
Investigations for oesophageal varices
Endoscopy (OGD) -shows dilated veins -also therapeutic U&Es (↑ Urea) FBC, group & screen, LFTs U&Es (↑ Urea)
Management of oesophageal varices
Resuscitation, IV fluids, blood transfusions
Pre-endoscopy
- terlipressin or ocreotide
- prophylactic Abx
Endoscopy
-variceal band ligation (1st line)
uncontrolled haemorrhage
-sengstaken-blakemore tubes
Transjugular intrahepatice portosystemic shunt (TIPSS)
-last resort
Prophylaxis of oesophageal varices
Propanolol
endoscopic vatical band ligation + PPI cover
Portalhypertension
pathological elevation of portal venous pressure from obstruction of portal blood flow which may be pre-hepatic (portal vein thrombosis), intra-hepatic (cirrhosis) or post-hepatic (right sided HF)
clinically significant if hepatic venous pressure gradient ≥10mmHg
most commonly due to cirrhosis
Presentation of portal hypertension
dilated veins at portosystemic anastomosis
- paraumbilical veins & epigastric veins → caput medusae
- rectal veins → hemorrhoidal or anorectal varices
- veins of the gastric fundus & distal 1/3 of the esophagus → gastric/oesophageal varices
Congestive splenomegaly
Transudative ascites
signs of liver failure (jaundice, spider naevi, palmar erythema)
hyper dynamic circulation (bounding pulse, ↓BP, warm peripheries)
Investigations of portal hypertension
FBC, U&Es, LFTs, clotting
abdo USS (splenomegaly, portal vein dilation, cavernous transformation of portal vein)
abdo CT
Hepatic venous pressure gradient ( ≥10mmHg)
Management of portal hypertension
beta blockers ± nitrates (↓ pressure)
salt restriction & diuretics
Transjugular intrahepatice portosystemic shunt (TIPSS)\
treat underlying cause or liver transplant
complications of Transjugular intrahepatice portosystemic shunt (TIPSS)
exacerbation of hepatic encephalopathy is a common complication
Ascites
pathological collection of fluid in the peritoneal cavity
on clinical examination ~1500ml detectable
on USS can detect volumes ≤500ml
Aetiology of ascites
~75% = cirrhosis ~15% = malignancy e.g. meigs syndrome with ovarian cancer or GI tract malignancy
others: Heart failure, nephrotic syndrome
Presentation of ascites
progressive abdominal distension
abdominal discomfort (secondary to distension)
↑ weight
early satiety
dyspnoea
shifting dullness on percussion (+ve if ~1500ml fluid)
peripheral/generalised oedema
Investigations for ascites
serum-ascites albumin gradient (SAAG)
≥11g/L or ≥1.1g/dL = transudate (portal hypertension)
<11g/L or <1.1g/dL = exudate (hypoalbuniaemia)
FBC, U&Es, LFTs, clotting, TFTs
abdo USS or abdo MRI/CT (may show underlying cause)
ascitic tap
-SAAG
-cell count (neutrophils >250 indicates SBP)
-RBCs (<1000 = normal, ↑ indicates malignancy)
Serum-ascites albumin gradient (SAAG)
Helps to determine underlying cause but requires ascitic tap
≥11g/L or ≥1.1g/dL = transudate
indicates portal hypertension
i.e. liver failure/cirrhosis, liver malignancy, right sided HF, constrictive pericarditis etc
<11g/L or <1.1g/dL = exudate
indicates hyporlbuniameia
i.e. nephrotic syndrome, severe malnutrition (e.g. kwashiorkor), infections, pancreatitis
Management of ascites
restrict salt intake (especially in cirrhosis)
diuretics
-spironolactone (1st line in cirrhosis), monitor K+
± loop diuretics e.g. furosemide
therapeutic paracentesis -give Human albumin solution if removing large volumes TIPSS prophylactic ABx (to prevent SBP) -ciprofloxacin/norofloxacin
Spontaneous bacterial peritonitis (SBP)
a bacterial infection of ascitic fluid in the absence of any identifiable intra-abdominal source of infection
may be due to bacteria spreading across intestinal wall
Aetiology of Spontaneous bacterial peritonitis (SBP)
most commonly E. Coli
otherwise Klebsiella
Presentation of Spontaneous bacterial peritonitis (SBP)
fever ascites abdo pain naseau & vomiting constipation/diarrhoea
Investigations for Spontaneous bacterial peritonitis (SBP)
ascitic tap -neutrophil count >250 cells/mm3 -ascitic fluid culture FBC blood cultures
Management of Spontaneous bacterial peritonitis (SBP)
empirical Abx (generally IV)
-1st line: IV cefotaxime
-2nd line: IV ceftriaxone/ciprofloxacin
consider human albumin solution
Hepatorenal syndorme (HRS)
development of acute renal failure in pts with severe liver disease, commonly associated with Spontaneous bacterial peritonitis (SBP) or other infections
diagnosis of exclusion generally
can be in acute or chronic liver failure
Presentation of Hepatorenal syndorme (HRS)
jaundice
ascites
features of liver failure
peripheral oedema
Diagnostic criteria for Hepatorenal syndorme (HRS)
Diagnostic criteria:
- cirrhosis
- creatinine >133
- absence of shock/absence of hypovolaemia
- no recent treatment with nephrotoxic drugs
- absence of parenchymal renal disease
Types of Hepatorenal syndorme (HRS)
HRS type 1: rapidly progressing associated with precipitant event e.g. infection creatinine doubles to >221 in <2 weeks very poor prognosis
HRS type 2:
gradual decline of renal function
associated with Na+ retention & refractory ascites
Treatment of Hepatorenal syndorme (HRS)
splanchnic vasoconstrictors e.g. terlipressin
human album solution
treat precipitating infection
TIPSS
Hepatic encephalopathy
a spectrum of neuropsychiatric abnormalities cause by acute/chronic hepatic insufficiency generally related to excess ammonia & glutamine absorption in the brain due to portosystemic shunting
precipitating events for hepatic encephalopathy
transjugular intrahepatic portosystemic shunting (TIPSS) infections e.g. SBP renal failure constipation GI bleed
Presentation of hepatic encephalopathy
confusion & altered level of consciousness
fatigue, lethargy, apathy, irritability
disorientation, memory loss, sleep impairment
socially aberrant behaviour
slurred speech, muscle rigidity, constructional apraxia
asterix (liver flap)
arrhythmic negative myoclonus
Grading of hepatic encephalopathy
I: irritability & sleep disturbances
II: confusion & inappropriate behaviour
III: incoherent, restless, somnolent but rousable, amnesia, disorientation
IV: coma
Management of hepatic encephalopathy
reducing gut nitrogen load
1st line : lactulose + rifamixin (sedentary prophylaxis)
2nd line enemas
Prophylaxis of hepatic encephalopathy
Rifamixin reduces recurrences
Hepatopulmonary syndrome
secondary to portal hypertension
triad of hepatic dysfunction, hyperaemia, extreme vasodilation of intrapulmonary vasculature
presents with dyspnoea, platypnoea (SOB better when lying flat), orthodeoxia (↓sats when going from lying to standing)
resolves after liver transplant
Portopulmonary hypertension
unexplained pulmonary hypertension in association with portal hypertension
often asymptomatic
requires echo & right heart catheterisation
treatment is liver transplant
Hepatocellular carcinoma (HCC)
a malignant usually solitary tumour of the liver often seen in pts with pre-existing cirrhosis or chronic hepatitis
~90% of all liver cancers (most common primary liver tumour)
Aetiology of Hepatocellular carcinoma (HCC)
chronic Hepatitis B or C infections (most common cause)
alcoholic liver disease
others: haemochromatosis, primary biliary cirrhosis
Epidemiology of Hepatocellular carcinoma (HCC)
more common in men (~4x)
usually seen age 65-70 yrs
Presentation of Hepatocellular carcinoma (HCC)
usually presents with symptoms of cirrhosis/liver failure
pruritus splenomegaly & hepatomegaly weight loss oesophageal varices jaundice hepatic encephalopathy ascties RUQ pain/tenderness spider naevi caput medusa flapping tremor
Screening for Hepatocellular carcinoma (HCC)
for pts at risk of HCC e.g. HBV/HCV or alcohol related cirrhosis
USS every 6-12 months ± Alpha fetoprotein (AFP)
Investigations for Hepatocellular carcinoma (HCC)
Serum AFP (↑) LFTs, FBC, Clotting liver USS (best initial investigation) contrast enhanced CT/MRI abdo liver biopsy
Tumour marker for Hepatocellular carcinoma (HCC)
Serum Alpha fetoprotein (AFP)
Management of Hepatocellular carcinoma (HCC)
tumour resection
-requires good liver function
liver transplant
-only very few pts suitable
Ablative therapy e.g. radio frequency ablation
-treatment fo choice in early stages
systematic chemotherapy
Chemoembolisation
-requires good liver function & no extra hepatic spread vascular invasion
Non alcoholic fatty liver disease (NAFLD)
Fatty liver disease developing in patients that do not consume alcohol in amounts considered harmful
most common cause of chronic liver disease in the developed world
Risk factors for Non alcoholic fatty liver disease (NAFLD)
obesity T2DM hyperlipidaemia jejunoileal bypass sudden weight loss/starvation metabolic syndrome HTN total parenteral nutrition
Presentation of Non alcoholic fatty liver disease (NAFLD)
often asymptomatic hepatomegaly obesity fatigue features of cirrhosis
Investigations for Non alcoholic fatty liver disease (NAFLD)
LFTs (all ↑, ALT > AST, i.e. AST:ALT ratio <1 )
-if AST:ALT ratio reverses (>1) may mean progression to cirrhosis
fasting lipids (↑)
liver USS (hyperechogenic)
Liver biopsy (only definitive test)
FBC, viral serology, iron studies, ceruloplasmin
Management of Non alcoholic fatty liver disease (NAFLD)
lifestyle changes (diet &exercise)
weight loss
monitoring of disease
Alcoholic related fatty liver disease
similar to Non alcoholic fatty liver disease (NAFLD) but in pts consuming harmful amounts of alcohol
Investigations
- gamma-GT (↑↑)
- AST:ALT ratio >2 (>3 almost exclusively sent in alcoholic liver disease)
Managed with drinking cessation
glucocorticoids are used in acute episodes of alcoholic hepatitis
Wilson’s disease (hepatolenticular degeneration)
autosomal recessive disease of copper accumulation & copper toxicity caused by mutations of ATP7b gene (part of biliary copper pathway)
i.e. disease of hepatic copper deposition
Genetics of wilson’s disease
autosomal recessive
mutations of ATP7b gene
Epidemiology of Wilson’s disease
RARE condition
onset usually age 10-25yrs
usually goes undiagnosed until combination of hepatitis, dementia & Parkinsonism causes clinical suspicion
Presentation of Wilson’s disease
Hepatic features:
-hepatitis, cirrhosis, hepatosplenomegaly, jaundice, portal hypertension, ascites
Neurological features
-basal ganglia degeneration, dysarthria, dystonia, parkinsonism, drooling, ataxia, wing beating tremor, asymmetric tremor (most common early neurological feature)
Psychiatric features:
-depression, behavioural change, irritability, cognitive impairment, psychosis
ophthalmic features:
-Kayser-Fleischer rings (green-brown rings in periphery of iris due to copper deposition)
Renal tubular acidosis (Fanconi syndrome)
blue nails
infertility
Investigations for Wilson’s disease
slit lamp examination
-for Kayser-Fleischer rings
Serum caeruloplasmin (↓) Total serum copper (↓) LFTs (deranged) urinary copper excretion (↑) Liver biopsy (↑parenchymal copper concentration)
Management of Wilson’s disease
monitor LFTs, coagulation, FBCs
1st line: Penicillamine (copper chelation)
-trientine hydrochloride (slowly becoming 1st line)
usually combined with Zinc (↓ copper absorption)
Haemochromatosis
multisystem disorder of iron absorption & metabolism resulting in iron accumulation
autosomal recessive mutation of the HFE gene
most common genetic disorder in white people
genetics of Haemochromatosis
autosomal recessive
mutation of the HFE gene
Presentation of Haemochromatosis
Early features:
-fatigue, lethargy, arthralgia, erectile dysfunction
Later features:
- liver (abdo pain, jaundice, cirrhosis)
- bronze pigmentation of skin
- diabetes mellitus
- cardiac failure (dilated cardiomyopathy)
- hypogonadism
- arthritis (especially of hands)
Investigations for Haemochromatosis
Joint X-rays (chonedrocalcinosis)
Ferritin (↑) serum iron (↑) Total iron binding capacity (TIBC) (↑) transferrin saturation (↑) ->55% in men, >50% in women
LFTs
-↑AST, ↑ALT
MRI (to measure liver iron content)
echocardiogram (dilated cardiomyopathy)
Genetic testing
-for 1st degree relatives of pt with confirmed disease/confirmed iron overload
Management of Haemochromatosis
1st line: phlebotomy/venesection
2nd line: desferrioxamine
Liver transplant in end stage liver disease
Autoimmune hepatitis
condition of unknown origin generally seen in young females, associated with other autoimmune conditions
presents with signs of chronic.acute liver disease & amenorrhoea
Investigations include LFTs (deranged, ↑ ↑ALT), serum antibodies, IgG (↑) and liver biopsy (key)
Managed with steroids & immunosuppressants e.g. azathioprine
Acute liver failure
rapid onset hepatocellular dysfunction
usually due to paracetamol overdose, acute fatty liver disease fo pregnancy, viral hepatitis (Hep A/B) or alcohol
presents with jaundice, coagulopathy (↑ prothrombin time), hypoalbuminaemia, hepatic encephalopathy and hepatorenal syndrome
Mangement is early liver transplant
Gallstones (cholelithiasis)
the presence of solid concretions in the gall bladder which may pass into the bile duct and cause obstruction
very common condition
in developed countries 90% of gallstones are made of cholesterol
Risk factors for gallstones
↑age FH of gallstones sudden weight loss diabetes oral contraception pregnancy female gender
Presentation of gallstones
mostly asymptomatic
biliary colic:
colicky RUQ pain
-worse after easting, worse after fatty food
-pain may radiate to R shoulder/intrascapular region
N&V
bloating
Investigations for gallstones
USS of RUQ (demonstrates stones)
-if -ve but high index of suspicion then repeat
ERCP or CT
Management of gallstones
expectant management if asymptomatic
ERCP (to remove stones)
elective laparoscopic cholecystectomy
Acute cholecystitis
acute gallbladder inflammation
one of the major complications of gallstones, developing in ~10%of symptomatic pts with gallstones
usually due too complete cystic duct obstruction (~90% of cases)
Risk factors for Acute cholecystitis
gallstones female gender ↑age obesity pregnancy Crohns disease hyperlipidaemia
Presentation of Acute cholecystitis
RUQ pain
- radiating to R shoulder/epigastric region
- severe & prolonged pain (>6h)
- worse after eating
Fever, malaise, N&V
Murphys sign +ve
- press on RUQ and ask pt to breath in
- +ve if elicits pain leading to arrestor inspiration
- only +ve if same manoeuvre in LUQ doesn’t cause pain
Investigations for Acute cholecystitis
USS (1st line investigation)
-shows thickened gallbladder walls, distended gallbladder and possibly gallstones
FBC (↑ WCC)
CRP (↑)
LFTs (usually normal)
consider MRI/CT/HIDA if USS inconclusive
Management of Acute cholecystitis
IV Abx analgesia e.g. morphine early laparoscopic cholecystectomy -within 1 week of diagnosis -gold standard
Acute/ascending cholangitis
an infection of the biliary tree typically secondary to biliary obstruction & stasis secondary to gallstones
may also be caused by malignancy affecting the biliary tree
causative organisms is usually E. Coli
Presentation of Acute/ascending cholangitis
Charcots triad:
- RUQ pain (maybe poorly localised abdo pain in elderly)
- Fever
- Jaundice
Raynauds pentad
- RUQ pain (maybe poorly localised abdo pain in elderly)
- Fever
- Jaundice
- hypotension (septic shock)
- confusion
Investigations for Acute/ascending cholangitis
FBC (↑WCC) ESR/CRP (↑) LFTs (↑bilirubin, ↑AST, ↑ALT, ↑ALP, ↑GGT) U&Es (↑creatinine, ↑urea) blood cultures amylase (may be ↑) USS abdo (dilated bile ducts ±gallstones) ERCP/CT scan
management of Acute/ascending cholangitis
IV ABx & IV fluids
analgesia
endoscopic retrograde cholangipancreatography (ERCP)
-after 24-48h to relieve any obstruction
Primary biliary cholangitis / Primary biliary cirrhosis (PBC)
chronic disease of the small intrahepatic bile ducts of autoimmune origin thats is characterised by destruction of interlobular bile ducts due to chronic inflammation
Conditions associated with Primary biliary cholangitis (PBC)
Sjogrens syndrome (up to 80% of pts)
Rheumatoid arthritis
systemic sclerosis
thyroid disease
Presentation of Primary biliary cholangitis (PBC)
initially asymptomatic fatigue, pruritus cholestatic jaundice, dark urine, pale stools hepatomegaly RUQ discomfort hyperpigmentation, xanthelasma cirrhosis (in advanced disease)
Investigations for Primary biliary cholangitis (PBC)
LFTs (↑ gamma-GT, ↑ALP, ↑bilirubin) ESR (↑) IgM (↑) anti-mitochondrial antibodies (AMA) M2 (+ve) abdo USS MRI cholangiopancreatography (MRCP)
Management of Primary biliary cholangitis (PBC)
1st line: ursodeoxycholic acid
cholestyramine for prurits
Vit ADEK supplements
Antibodies associated with Primary biliary cholangitis (PBC)
98% of pts have anti-mitochondrial antibodies (AMA) M2 (+ve)
smooth muscle antibodies (+ve in 30%)
anti-nuclear antibodies
Primary sclerosis cholangitis (PSC)
a progressive chronic inflammatory disease of the intrahepatic & extra hepatic bile ducts characterised by inflammation & fibrosis resulting in diffuse multi-focal stricture formation
Primary sclerosis cholangitis (PSC) associated conditions
strongly associated with ulcerative colitis
-~80% of PSC patients have UC
NB only 5% of UC pts have PSC
presentation of Primary sclerosis cholangitis (PSC)
cholestasis
-jaundice, scleral icterus, pruritus, pale stools, dark urine
-fatigue
-may cause acute cholangitis (fever, RUQ pain, jaundice)
weight loss
hepatomegaly
cirrhosis (in late stage)
Investigations for Primary sclerosis cholangitis (PSC)
MRCP (gold standard) ERCP LFTS (↑ALP, ↑gamma-GT, ↑bilirubin, AST/ALT slightly ↑) cholesterol (↑) IgM (↑) p-ANCA (may be +ve)
Management of Primary sclerosis cholangitis (PSC)
ursodeoxycholic acid (1st line)
balloon dilatation of strictures causing recurring cholangitis
cholestyramine for pruritis
Vit ADEK supplements
liver transplant is only curative treatment
Crohn’s disease
an inflammatory bowel disease (IBD) of unclear aetiology which manifests anywhere in the GI tract characterised by transmural granulomatous inflammation & skip lesions
often affects terminal ileum & colon
Risk factors for Crohn’s disease
Family history
smoking (smokers tend to have more aggressive disease)
HLA-B27
Presentation of Crohn’s disease
generally presents with episodes of acute exacerbation interspersed with remission/less active disease
weight loss, fever, anorexia, fatigue
GI symptoms:
chronic diarrhoea, abdo pain/discomfort, perianal disease (ulcers, skin tags), fistulas, features of malabsorption (e.g. anemia)
Extra intestinal symptoms
- enteropathic arthritis (usually lower body, asymmetrical, or scaroilitis/ankylosing spondylitis)
- uveitis, episcleritis
- pyoderma gangrenosum
- clubbing, erythema nodosum
Investigations for Crohn’s disease
Diagnostic (1st line)
- endoscopy (deep ulcers, skip lesions, cobllesotning, oedema)
- tissue biopsy (transmural inflammation, non-caveating granulomas)
FBC (↓Hb) CRP (↑ in active disease) faecal calprotectin (↑ in active disease) stool MC&S CT/MRI with oral contrast
Investigations for Crohn’s disease
Diagnostic (1st line)
- endoscopy, both colonoscopy & OGD (deep ulcers, skip lesions, cobllesotning, oedema)
- tissue biopsy (transmural inflammation, non-caveating granulomas)
FBC (↓Hb) CRP (↑ in active disease) faecal calprotectin (↑ in active disease) stool MC&S CT/MRI with oral contrast
Management of Crohn’s disease
Inducing remission:
glucocorticoids (1st line), mesalazine (2nd line)
Maintaining remission:
azathioprine/mercaptopurine (1st line), methotrexate (2nd line)
Surgery
~80% of pts will have surgery,
e.g. bowel resection ± stomas, fistula corrections or stricturoplasty
Inducing remission in Crohn’s disease
1st line: Glucocorticoids IV/PO
2nd line: 5-ASA drugs e.g. mesalazine
±azathioprine/mercaptopurine/methotrexate (never as mono therapy)
infliximab for refractory disease or fistulating crohn’s
Maintaining remission in Crohn’s disease
1st line: azathioprine/mercaptopurine (assess TPMT activity before starting)
2nd line: methotrexate
Ulcerative colitis (UC)
an inflammatory bowel disease (IBD) characteristically involving chronic inflammation of the mucosa of the rectum/colon/caecum
NB always starts at the rectum so rectum is most common site
Ulcerative colitis (UC) epidemiology
most common form of IBD
peak incidence age 15-25 yrs
Risk factors for Ulcerative colitis (UC)
HLA-B27
white ehtnicity
FH of IBD
Presentation of Ulcerative colitis (UC)
generally relapsing and remitting course
bloody diarrhoea ± mucous, faecal urgency ,abdo pain (mainly LLQ), cramps, tenesmus, rectal bleeding, constipation, weight loss, malaise
Extra-intestinal disease
- erythema nodosum & pyoderma gangrenosum
- primary sclerosis cholangitis (PSC)
- anterior uveitis
- sacroilitis, ankylosing spondylitis
Investigations for Ulcerative colitis (UC)
- colonoscopy (rectal involvement, continuous uniform involvement, widespread ulceration, red/raw mucosa, normal terminal ileum, friable mucosa)
- biopsy (mucin depletion, diffuse mucosal atrophy, crypt abscesses, neutrophil infiltration limited to mucosa/submucosa)
FBC (↑WCC, ↓Hb)
ESR/CRP (↑)
faecal calprotectin (↑)
stool analysis
Management of Ulcerative colitis (UC)
Inducing remission
PO/topical 5-ASA agents e.g. mesalazine
if extensive PO 5-ASA plus steroids
Maintaining remission
1st line 5-ASA agents PO/topical
if severe then azathioprine/mercaptopurine
Biologicals e.g. infliximab/tofacitinib
surgery:
colectomy is curative (~30% of pts have this procedure)
Difference for Ulcerative colitis (UC) and Crohn’s
Crohn’s can present anywhere in GI tract,
UC always starts at rectum and is limited to large intestines,
Crohn’s has skip lesions
UC is continuous disease with no skip lesions
Crohns has normal diarrhoea
UC may have bloody diarrhoea
Crohns is transmural inflammation in all layers
UC is inflammation limited to mucosa & submucosa
Methotrexate can be used in Crohn’s
Methotrexate is not used in UC
Maintaining remission in Ulcerative colitis (UC)
1st line: topical/oral aminosalicylates e.g. Sulfasalazine/Mesalazine
if severe flare/>2 flares in past year = azathioprine/mercaptopurine
Irritable bowel syndrome (IBS)
A chronic condition characterised by abdo pain associated with bowel dysfunction
its defined by a symptom based diagnostic criteria in the absence of a detectable organic cause
Epidemiology for Irritable bowel syndrome (IBS)
affects 10-20% of population
more common in women
most prevalent in ages 20-30yrs
Presentation of Irritable bowel syndrome (IBS)
≥ 6 months of either: abdo pain/discomfort, bloating, change in bowel habit
considered +ve if abdo pain received by defecation or associated with altered bowel habit/frequency or stool form
≥2 of the following as well: altered passage of stool (straining/urgency/incomplete evacuation), bloating, distension, symptoms worsened by eating, passage of mucus
other features include lethargy, nausea, backache
Investigations for Irritable bowel syndrome (IBS)
clinical diagnosis via ROME IV criteria
consider work up including FBC, U&Es, LFTs, CRP, coeliac screen, faecal calprotectin and CA125
Management of Irritable bowel syndrome (IBS)
Lifestyle e.g. more fibre, exercise etc
Pharmacological:
1st line:
-Pain: give antispasmodics e.g. mebeverine/alverine
-constipation: bulk forming laxatives but avoid lactulose
-diarrhoea: loperamide
NB if no response to conventional laxatives try linaclotide
2nd line:
-TCAs e.g. amitriptyline
Gastro-oesophageal reflux disease (GORD)
symptoms or complications resulting from the reflux of gastric contents into the oesophagus or beyond into the oral cavity/lungs
Epidemiology of Gastro-oesophageal reflux disease (GORD)
2-3x more common men
Epidemiology of Gastro-oesophageal reflux disease (GORD)
2-3x more common men
Risk factors for Gastro-oesophageal reflux disease (GORD)
smoking stress obesity pregnancy hiatus hernia caffeine alcohol
Presentation of Gastro-oesophageal reflux disease (GORD)
heartburn (retrosternal burning pain) -worse after meals, lying down, straining regurgitation dysphagia odynophagia bloating early satiety non cardiac chest pain dyspepsia halitosis non-productive night time cough
Investigations for Gastro-oesophageal reflux disease (GORD)
Proton pump inhibitor (PPI) trial
-4 weeks, +ve if symptoms improve
Oesophagogastroduodenoscopy (OGD)
-indicated if alarm symptoms e.g. dysphagia/odynophagia, weight loss
Barium swallow (may show hiatus hernia)
oesophageal pH monitoring
-pH <4 frequently is abnormal
Management of Gastro-oesophageal reflux disease (GORD)
lifestyle interventions
- weight loss
- stop smoking
- ↓ alcohol intake
- small regular meals
- avoid eating/alcohol within 3h of bedtime
PPI trial for 4 weeks e.g. lansoprazole
- if no response then double dose
- if effective then continue PPI
- considering adding H2RA e.g. ranitidine if still symptomatic
Barretts oesophagus
a change in the normal oesophageal squamous epithelium to the columnar epithelium normally found in the stomach
a metaplastic process
associated with GORD
Epidemiology of Barretts oesophagus
seen in ~5% of pts with GORD
more common in men
more common in caucasians
Presentation of Barretts oesophagus
often asymptomatic
usually GORD symptoms i.e. reflux, heartburn etc
symptoms of oesophageal stricture e.g. dysphagia
Risk factors for Barretts oesophagus
GORD male gender smoking central obesity hiatus hernia
Investigations for Barretts oesophagus
OGD
-visible colonisation, oesophagitis, inflammation
Biopsy (gold standard)
-area of columnar lined epithelium in the oesophagus at a level superior to the gastro-oesophageal junction
Management of Barretts oesophagus
endoscopic surveillance with biopsy (every 3-5 years)
high dose PPI
if dysplasia identified
- endoscopic mucosal resection
- radio frequency ablation
Oesophageal cancer
cancer of the oesophagus
2 common types
- adenocarcinoma (most common in developed world)
- squamous cell carcinoma
more common in men, usually aged >75yrs
generally has poor prognosis
Risk factors for oesophageal cancer
smoking GORD/Barretts oesophagus (for adenocarcinoma) strictures (for SCC) obesity (for adenocarcinoma) Plummer Vinson syndrome (for SCC)
Locations of oesophageal cancers
adenocarcinoma: tends to be in lower 1/3 of oesophagus, near gastro-oesophageal junction
Squamous cell carcinoma : tends to be in upper 2/3 of oesophagus
Presentation of oesophageal cancer
dysphagia vomiting weight loss anorexia odynophagia hoarseness retrosternal pain
2 week wait criteria for suspect oesophageal cancer
unexplained dysphagia at any age
age >55 + weight loss and upper abdo pain/reflux/dyspepsia
Investigations for oesophageal cancer
OGD with biopsy
CT chest/abdo/pelvis
FBC, U&Es, LFTs, CRP
Management of oesophageal cancer
Curative (depends on staging)
- neoadjuvant chemo / adjuvant chemo
- surgical resection (total or subtotal oesophagectomy)
Palliation
- stent placement
- chemo
- endoscopic therapy
NB a complication of surgery includes anastomotic leak leading to mediastinitis
Mallory-Weiss tear
acute upper GI bleeding secondary to mucous membrane lacerations at the gastro-oesophageal junction usually after forceful/prolonged vomiting
associated with alcoholism/excessive alcohol intake
presents with haematemesis after a bout of vomiting/retching ± signs of shock
Investigated & treated with OGD
Plummer Vinson syndrome
triad of iron deficiency anaemia, atrophic glossitis and oesophageal webs/strictures usually seen in middle aged women
presents as painless intermittent dysphagia, lethargy, tiredness
investigated with FBC (↓Hb), barium swallow (webs/strictures)
managed with iron supplementation, endoscopic dilation
Boerhaaves syndrome
spontaneous oesophageal rupture (usually distal) secondary to repeated episodes of vomiting
presents with sudden onset, severe chest pain and vomiting
investigated with CT contrast swallow
managed with thoracotomy & lavage + primary repair if within 12h or T tube insertion if >12h ago
Peptic ulcer disease (PUD)
the presence of one or more ulcerative lesions in the stomach or duodenum
break in mucosal lining should be >5mm
Aetiology of Peptic ulcer disease (PUD)
H. Pylori infection (most common cause)
chronic NSAID use
SSRIs/corticosteroids/bisphosphonates
Zollinger-Ellison syndrome (rare, gastrin secreting neuroendocrine tumour)
Conditions associated with H. Pylori infection
Peptic ulcer disease (PUD)
Gastric MALT lymphoma (good prognosis)
Presentation of Peptic ulcer disease (PUD)
generally asymptomatic or presenting with complications such as perforation/bleeding
abdo pain (usually epigastric)
-gastric ulcer: aggravated by eating
-duodenal ulcer: received by eating/worse when hungry
indigestion, reflux, bloating, nausea and vomiting
dyspepsia, oral flatulance, intolerance of fatty food
Presentation of gastric ulcer
epigastric pain aggravated by eating
Presentation of duodenal ulcer
epigastric pain when hungry
pain is relieved by eating
Investigations for Peptic ulcer disease (PUD)
H. Pylori
-urea breath test, still antigen test (if +ve then H. Pylori likely to be the cause)
FBC (↓ Hb if bleeding)
OGD* (demonstrates ulcers)
fasting serum gastrin (↑ in Zollinger-Ellison syndrome)
NB OGD is gold standard
Management of Peptic ulcer disease (PUD)
stop NSAIDs (if suspected cause)
H.Pylori test -ve:
- PPIs until ulcer healed
- reevaluate after 4-8 weeks
H.Pylori test +ve:
- eradication therapy (triple therapy)
- PPI + amoxicillin + clarithromycin/metronidazole
- if penicillin allergy then PPI+ clarithromycin+metronidazole
Complications of Peptic ulcer disease (PUD)
Bleeding (acute)
- most common complication, especially if posterior ulcers
- presents with haematemesis, shock, anaemia
- clinical diagnosis ± OGD
- managed with IV PPI & endoscopic ligation
Perforation
- presents with sudden diffuse abdo pain, rigidity, peritonitis and shock
- consider CXR/AXR to show free air under diaphragm
- management includes NBM & urgent surgical repair
Upper GI bleed
refers to a GI bleed whose origin is proximal to the ligament of Treitz at the duodenojejunal junction
more common than lower GI bleed
Aetiology of Upper GI bleed
peptic ulcer disease (~25%) oesophagi's gastritis/erosions varices malignancy Mallory-weiss tear
~20% no aetiology is found
Presentation of Upper GI bleed
haematemesis
malaena
signs of shock (hypotension, tachycardia, tachypnoea)
Scoring of Upper GI bleed
Blatchford score
- consists of urea, Hb, sBP, HR, malaria, syncope, hepatic disease & HF
- used pre-endoscopy to assess need for intervention
- score of 0 = consider discharge
- score of ≥1 pt at risk fo requiring intervention
Rockall score
- used post endoscopy
- identifies risk of adverse outcomes
Pre-endoscopic scoring system for Upper GI bleed
Blatchford score
- consists of urea, Hb, sBP, HR, malaria, syncope, hepatic disease & HF
- used pre-endoscopy to assess need for intervention
- score of 0 = consider discharge
- score of ≥1 pt at risk fo requiring intervention
Post-endoscopy scoring system for Upper GI bleed
Rockall score
- used post endoscopy
- identifies risk of adverse outcomes
Investigations for Upper GI bleed
FBC, group & screen, cross match, coagulation, LFTs
U&Es (↑ urea)
CXR & AXR
endoscopy
-immediately after resuscitation if severe bleed
-within 24h for all pts
Management of Upper GI bleed
Resuscitation & reversal of anticoagulation
Non variceal bleed:
- 1st line: endoscopic therapy (thermal coagulation, clips ± adrenaline)
- endoscopy can be repeated if necessary
- PPIs post endoscopy
- 2nd line: interventional radiology + embolisation
Variceal bleeds:
- terlipressin & prophylactic Abx at presentation
- 1st line: endoscopic band ligation of oesophageal varices or injections of N-butyl-2-cyanoacrylate for gastric varices
- Sengstaken-Blakemore tube if uncontrolled haemorrhage
- transjugular intrahepatic portosystemic shunts (TIPSS) as last resort
Feature indicative of Upper GI bleed
↑ Urea is indicative of upper GI bleed
this is due to the ‘protein meal’ of blood in the stomach
Management of variceal upper GI bleed
terlipressin & prophylactic Abx at presentation
1st line:
- endoscopic band ligation of oesophageal varices
- injections of N-butyl-2-cyanoacrylate for gastric varices
uncontrollable haemorrhage
- Sengstaken-Blakemore tube
- transjugular intrahepatic portosystemic shunts (TIPSS)
Management of non variceal upper GI bleed
1st line:
- endoscopic therapy (thermal coagulation, clips ± adrenaline)
- can be repeated if necessary
- PPIs post endoscopy
2nd line:
interventional radiology + embolisation
Prophylaxis of variceal bleeding
Propanolol
Endoscopic band ligation with PPI cover
Lower GI bleed
a wide clinical spectrum from small bleeding to major haemorrhage
incidence increases with age
Aetiology of Lower GI bleed
Diverticular disease (15-40%) Meckels diverticulum colonic angiodysplasisa (common in older people) ischaemic colitis colonic cancer haemorrhoidal bleeding
Presentation of Lower GI bleed
Haematochezia (may be present in massive upper GI bleed)
- frank passage of blood PR
- the darker the blood the more distal the bleed from the rectum
malaena is rare
signs of shock (hypotension, tachycardia, tachypnoea)
Investigations for Lower GI bleed
colonoscopy after bowel prep (OGD if colonoscopy -ve)
PR examination
CT angiography
FBC, coagulation, U&Es
Management of Lower GI bleed
Resuscitation as necessary
1st line: supportive management
2nd line: endoscopic cauterisation/band ligation/clipping
NB generally no hyper acute management, can often refer to specialist
Pancreatic cancer
generally refers to primary pancreatic ductal adenocarcinoma which accounts for ~85% of all pancreatic neoplasms
Risk factors for pancreatic cancer
smoking FH of pancreatic cancer obesity diabetes chronic pancreatitis
familial cancer syndromes
- Peutz -Jeghers syndrome
- HNPCC (Lynch syndrome)
- MEN type I
pathognomonic presentation of pancreatic cancer
Painless jaundice is pancreatic cancer until proven otherwise
Epidemiology of pancreatic cancer
tends to present late & metastasis early
poor prognosis
only ~25% survive for ≥1 year after diagnosis
usually seen above age 75
Presentation of pancreatic cancer
painless jaundice (pathognomonic) -if painless jaundice + non tender enlarged gallbladder =courvoisiers signs
poor appetite, weight loss, fatigue malabsorption, pursuits, diarrhoea steatorrhoea, pale stools atypical back pain abdo pain (like a belt around abdomen) migratory thrombophlebitis (Trousseau sign)
Investigations for pancreatic cancer
Abdo USS (pancreatic mass, dilated bile ducts)
pancreatic protocol CT (mass in pancreas & metastasis)
LFTs (↑bilirubin, ↑ALP, ↑GGT, AST/ALT normal)
Ca 19-9 (+ve)
ERCP or MRCP
Management of pancreatitis
Whipples resection (pancreaticoduodenectomy) + adjuvant chemo
Palliative
chemo & radiotherapy, ERCP + stent placement
NB only ~20% suitable for surgery at diagnosis
Tumour marker for pancreatic cancer
Ca 19-9
Common metastasis sites of pancreatic cancer
Liver
Peritoneum
abdominal viscera
lungs
Gastric cancer
5th most common cancer world wide and 3rd leading cause of cancer death
~95% are adenocarcinomas
more common in men, usually over age 75
Risk factors for Gastric cancer
H. Pylori male gender smoking diet (high in salt) atrophic gastritis FH of gastric cancer
Presentation of Gastric cancer
often asymptomatic early on
Gastric symtpoms:
- Nausea, loss of appetite
- dyspepsia, weight loss, vomiting, early satiety
- vague abdo pain
Signs of advanced disease
- virchows node (L supraclavicular lymphadenopathy)
- Sister Mary joseph node (palpable umbilical nodule)
- hepatomegaly, ascites
- acanthosis nigricans (strongly associated with gastric cancer)
Investigations for Gastric cancer
endoscopy with biopsy
-may show signet ring cells
CT chest/abdo/pelvis
FBC, LFTs, U&Es
Management of Gastric cancer
Surgical resection:
- if early: endoscopic mucosal resection
- otherwise partial or total gastrectomy ± lymphadenectomy
post resection can perform a Roux-en-Y gastric bypass to reconstruct gastric passage
usually also neoadjuvant or adjuvant chemo
Colorectal cancer
mostly adenocarcinomas that develop from polyps
often locally invasive
4th most common cancer & 2nd most common cause of cancer death
usually diagnosed age 65-75 yrs
Most common site of metastasis for colorectal cancer
Liver
other sites e.g. brain/lungs/bones are uncommon if liver mets not present
Most common site of Colorectal cancer
Rectum
Risk factors for Colorectal cancer
FH of colorectal neoplasia IBD Polyposis syndromes HNPCC (lynch syndrome) obesity smoking alcohol abuse diabetes
Presentation of Colorectal cancer
Right sided Cancer:
weight loss, anaemia, occult bleeding, RIF mass, malaena, diarrhoea,
more likely to be advanced disease at presentation
Left sided Cancer:
colicky pain, rectal bleeding, bowel obstruction, tenesmus, LIF mass, early change in bowel habit, blood in stool
General:
weight loss, night sweats, fatigue, abdo discomfort
change in bowel habit
Metastasis:
jaundice, hepatomegaly
Rectal cancer:
haematochezia, ↓ stool caliber (pencil shaped stools), rectal pain, tenesmus, flatulence, faecal incontinence
Investigations for Colorectal cancer
FBC (↓ Hb), LFTs (abnormal if liver mets), U&Es
colonoscopy (to confirm diagnosis)
CT colonography (alternative to colonoscopy)
CT Chest/Abdo/Pelvis (staging)
carcinoembryonic antigen (CEA)
-throughout treatment & remission to monitor for relapse
Screening for Colorectal cancer
one off flexible sigmoidoscopy offered to all adults aged 55yrs (NB abandoned due to covid)
Faecal immunochemical test (FIT) screening
- offered every 2yrs to all men & women aged 60-74 yrs in england
- if FIT test abnormal offer colonoscopy
Referral criteria for suspected colorectal cancer
2 week wait:
- ≥40 y/o with unexplained weight loss & abdo pain
- ≥50y/o with unexplained rectal bleeding
- ≥60y/o with Iron deficiency anaemia or a change in bowel habit
- FIT test showing occult blood
- consider if pts < 50y/o with rectal bleeding + unexplained abdo pain/change in bowel habit/iron deficiency anaemia or if unexplained rectal mass/ulceration
NB if the criteria is not met then send for FIT test
Management of Colorectal cancer
Surgical:
- Right sided hemicolectomy if caecum/proximal transverse colon
- Left hemicolectomy if distal transverse colon/descending colon
- sigmoid colectomy if sigmoid colon
- anterior resection if low sigmoid colon/high rectal
- abdomino-perineal resection of lowe rectal
often with adjuvant/neoadjuvant chemo
if possible then liver mets can also be surgically removed
Presentation of Left sided colorectal cancer
colicky pain, rectal bleeding, bowel obstruction, tenesmus, LIF mass, early change in bowel habit, blood in stool
Presentation of Rectal cancer
haematochezia, ↓ stool caliber (pencil shaped stools), rectal pain, tenesmus, flatulence, faecal incontinence
Colonic polyps
polyps are abnormal colonic mucosal outgrowths commonly found in people over the age of 50
seen in younger people in hereditary polyposis syndromes
~70% of polyps are adenomas
Presentation of colonic polyps
mostly asymptomatic (so may present as colon cancer)
if symptomatic:
haematochezia , change in bowel habit, mucous in stool
palpable rectal polyps on PR
Investigations for colonic polyps
colonoscopy + biopsy
double contrats barium enema
CT colonography
FIT testing, Hb
Management of colonic polyps
snare polypectomy if ≤5mm in size
endoscopic mucosal resection if large sessile polyps
surgical resection
-if >2cm / suspected malignancy / familial polyposis syndromes
Hereditary polyposis syndromes
Familial adenomatous polyposis MYH associated polyposis Peutz-Jeghers syndrome Juvenile polyposis Cowden sydrome
Hereditary polyposis syndromes
Familial adenomatous polyposis MYH associated polyposis Peutz-Jeghers syndrome Juvenile polyposis Cowden sydrome
Familial adenomatous polyposis
autosomal dominant mutation in APC gene
typically presents age 10-30yrs
~100% chance of developing cancer
on colonoscopy shows >100 polyps
treated with prophylactic proctocolectomy with ill-pouch-anal anastomosis and 3 yearly endoscopic surveillance
MYH associated polyposis
autosomal recessive mutation of MUTYH gene
<100 polyps seen on endoscopy
treated with prophylactic proctocolectomy with ill-pouch-anal anastomosis
Peutz-Jeghers syndrome
autosomal dominant mutation of STK 11 gene
presents with harmatomatous polyposis and the defining feature of mucocutaneous pigmentation of the lips/buccal mucosa/genitlia/palms/soles
often presents with small bowel obstruction
on endoscopy there is multiple harmatomatous polyps throughout entire GI tract
managed with polyp excision & 3 yearly endoscopic surveillance
Juvenile polyposis
onset within first decade of life
presents with Gi bleeding & anaemia
Cowden syndrome
autosomal dominant mutation of PTEN gene
presents with multiple GI polyps and skin manifestations (hyperkeratosis & papules)
associated with breast cancer & thyroid disorders
Haemorrhoids (piles)
Haemorrhoidal cushions are normal anatomical structures within the anal canal, which may enlarge & protrude outdid the anal canal
Types of Haemorrhoids
internal (originate above dentate line)
external (originate below dentate line)
Risk factors for Haemorrhoids
excessive straining e.g. chronic constipation
extended periods of sitting
pregnancy
low fibre diet
Presentation of Haemorrhoids
painless rectal bleeding
-usually bright red bleeding at end of defecation
perianal pain/discomfort
internal haemorrhoids tend to be painless
external haemorrhoids tend to be painful perianal masses
Investigation for Haemorrhoids
PR examination
shows tenderness, masses and bleeding
Management of Haemorrhoids
↑dietary fibre ↑fluid intake bulk forming laxatives simple analgesia for pain topical steroids/local anaesthetics from symptom relief
rubber band ligation
haemorhoidectomy
-reserved for large symptomatic haemorrhoids
Small bowel obstruction
a mechanical disruption of the potency of the GI tract which is a medical emergency requiring early diagnosis & intervention
Risk factors for Small bowel obstruction
previous abdominal surgery
hernias
foreign body ingestion
intestinal malignancy
Aetiology of Small bowel obstruction
intra-abdominal adhesions (most common) inguinal hernia with incarceration other incarcerated hernias merckels diverticulum strictures (from Crohns) gallstone ileus tumours appendicits
Presentation of Small bowel obstruction
diffuse central abdo pain
nausea
bilious vomiting
complete constipation (failure to pass flatulence or stool)
abdo distensions (resonant on percussion)
tinkling bowel sounds
Investigations for Small bowel obstruction
Plain AXR (distended loops of bowel with fluid level) CT abdo/pelvis (definitive diagnosis) ABG, CRP, FBC, U&Es, LFTs, group&save
Management of Small bowel obstruction
DRIP & SUCK
- NBM (nil by mouth)
- IV fluids
- NG tube with free drainage
explorative laparotomy with management of obstruction cause
Large bowel obstructions
complete or partial mechanical interruption of flow of intestinal contents
surgical emergency
Aetiology of Large bowel obstruction
~60% colorectal malignancy
~20% diverticular strictures
~5% volvulus
Risk factors for Large bowel obstruction
colorectal adenomas/polyps current/previous malignancy IBD diverticular disease current/previous hernia previous abdo surgery
Presentation of Large bowel obstruction
intermitten abdo pain significant abdo distension nausea & vomiting total constipation high pitched bowel sounds tympanic percussion empty rectum
Investigations for Large bowel obstruction
AXR (1st line)
CT abdo/pelvis (dilation, shows underlying cause)
FBC, U&Es, group & screen
Management of Large bowel obstruction
Drip & suck
- NBM
- IV fluids
- NG tube with free drainage
explorative laparotomy
NB if surgery not indicated trial drip & suck for 72h
Volvulus
defined as a twisting of a loop of bowel on its mesentery most commonly affecting the sigmoid colon (~80%), then caecum (~20%)
one of the most common causes of intestinal obstruction
Type of volvulus
Sigmoid volvulus:
-associated with older pts & chronic constipation
Caecal volvulus:
-tends to be younger pts
Presentation fo volvulus
episodes of abdo pain relieved by explosive passage of stool/gas
slowly progressing symptoms of bowel obstruction
bowel ischaemia (tachycardia, hypotension, peritonits, haematochezia)
Bowel perforation (loss of dullness on percussion)
Investigation for volvulus
AXR
- sigmoid volvulus = coffe bean sign
- caecal volvulus = kidney bean sign
CT abdo pelvis
-sigmoid volvulus = whirl sign
Barium eneam
-birds beak sign
Management of volvulus
Sigmoid:
rigid sigmoidoscopy with recatl tube insertion
Caecal:
right hemicolectomy often needed
Toxic megacolon
toxic colitis with a megacolon (distension >6cm) is often refereed to as a toxic megacolon
usually due to C. diff infection or IBD if non infectious
Presentation of Toxic megacolon
bloody diarrhoea, vomiting
abdo distension & pain
sepsis (fever, hypotension, tachycardia, dehydration)
Investigations for Toxic megacolon
FBC (↑WCC) U&Es (↓K+), ESR/CRP (↑)
AXR
-loss of haustration, multiple air fluid levels, dilated colon
contrast CT
-rules out mechanical obstruction
Management of Toxic megacolon
NBM, NG tube & IV fluids (Drip & suck)
correct electrolyte imbalance
broad spectrum ABx
surgery if no response to medical treatment within 24-72h
Abdominal aortic aneurysm (AAA)
a focal dilatation of the abdominal aorta by >1.5x its expected diameter (generally >3cm)
originates inferior to renal arteries in 90% of cases
Risk factors of Abdominal aortic aneurysm (AAA)
↑age smoking* atherosclerosis hypercholesterolaemia FH of AAA hypertension
Presentation of unruptered Abdominal aortic aneurysm (AAA)
generally asymptomatic (i.e. incidental finding)
back pain
pulsate abdominal swelling
bruit on auscultation
Presentation of ruptured Abdominal aortic aneurysm (AAA)
hypovolaemic shock sudden onset severe tearing back/abdo pain painful pulsatile mass Grey Turner sign (flank ecchymosis) Cullen sign (periumbilical ecchymosis) syncope
NB mortality is ~80%
Investigations for Abdominal aortic aneurysm (AAA)
abdo USS (aorta diamete >3cm)
CT angiography (especially if pt symptomatic)
Management of Abdominal aortic aneurysm (AAA)
Asymptomatic AAA <5.5cm: monitor with USS
- 3.0-4.4 cm annually
- 4.5-5.4cm 3 monthly
Management of Abdominal aortic aneurysm (AAA)
Asymptomatic AAA <5.5cm: monitor with USS
- 3.0-4.4 cm annually
- 4.5-5.4cm 3 monthly
consider elective repair (endoscopic or open) if symptomatic AAA, AAA >5.5cm, AAA >4.0cm & growing >1cm in one year
Manage lifestyle e.g. smoking and HTN
Epidemiology of Abdominal aortic aneurysm (AAA)
more common elderly men
usually aged >60yrs
NB rupture of AAA is more common in women
Management of ruptured Abdominal aortic aneurysm (AAA)
resuscitation & blood transfusion
end-vascular aneurysm repair (EVAR) or open surgical repair within 90 min
Monitoring for asymptomatic Abdominal aortic aneurysm (AAA)
considered if asymptomatic AAA <5.5cm
monitor with USS
- 3.0-4.4 cm annually
- 4.5-5.4cm 3 monthly
Constipation
a ploy somatic heterogenous disorder defined by the infrequent of difficult passage of stool
- usually defined as ≤3 bowel movements/week
- or difficult passage of stool e.g. straining/discomfort
Aetiology of constipation
low fibre diet, immobility, dehydration IBS, old age
anal fissure, rectal prolapse, strictures
hypothyroidism, hypercalcaemia, opioid analgesia
iron supplements
chronic laxative abuse
Investigations for constipation
consider investigations if >40y/o, recent change of bowel habit, associated symptoms e.g. weight loss, rectal bleeding, mucous discharge or tenesmus
FBC, U&Es, Ca2+, TFTs
colonoscopy, AXR
Management of constipation
mobilise pt
↑ fluid intake
↑ fibre intake
Pharmacological i.e laxatives (use for short duration if above don’t work)
- bulk forming e.g. sterculia, ispagula husk
- stool softeners e.g. archis oil enema (for impaction)
- stimulants e.g. senna, docusate
- osmotics e.g. lactulose, macrogol.movicol (can be used long term for chronic constipation)
- enemas e.g. phosphate enema
Abdominal wall hernias
protrusion of an organ or the fascia of an organ through the wall of the cavity that normally contains them
associated with obesity, ascites, ↑age, previous surgery
Abdominal wall hernias
protrusion of an organ or the fascia of an organ through the wall of the cavity that normally contains them
associated with obesity, ascites, ↑age, previous surgery
Most hernias are clinically diagnosed but may be confirmed with USS
Inguinal hernia
protrusion abdo/pelvic contents into the inguinal canal and out through the external inguinal ring
Types:
- indirect = protrusion through internal inguinal ring, ~80% of inguinal hernias, more common in children
- direct = protrusion through weakness in posterior wall of inguinal canal, more common in the elderly
Type sof inguinal hernia
indirect
- protrusion through internal inguinal ring
- ~80% of inguinal hernias
- more common in children
direct
- protrusion through weakness in posterior wall of inguinal canal
- more common in the elderly
Presentation of inguinal hernia
mass in inguinal region (groin lump)
- superior & medial to the pubic tuberosity
- disappears on pressure/when pts lies down
discomfort/ache worse on exercise/activity
Management of inguinal hernia
surgical repair of hernia
Complications of hernias
incarceration of hernia
- irreducible hernia with normal overlying skin
- associated with bowel obstruction
- can attempt manual reduction prior to surgery
strangulated hernia
- sudden severe groin pain due to constriction & ischaemia
- associated with bowel obstruction
- overlying skin is warm, erythematous, tender
NB both these require emergency surgical repair
Femoral hernias
protrusion of abdominal viscera into the femoral canal
accounts for ~5% of abdominal hernias
more common in women, especially if multiparous
Presentation of femoral hernia
lump in groin
- lateral & inferior to pubic tubercle
- swells on coughing/straining
- typically non reducible
Management of femoral hernia
elective surgical repair ASAP due to strangulation risk
DO NOT used hernia trusses
NB risk of strangulation much higher than for inguinal hernias
Incisional hernia
herniation of abdominal content through and abdominal wall defect created during previous surgery, generally occur within 3 years of surgery
midline laparotomies pose highest risk
presents as mass/protrusion at site of incisional scar
generally managed conservatively unless symptomatic
Umbilical hernia
very common in infants, but accounts for ~5% of adult abdominal wall hernias
presents adjacent to umbilical orfice, pushing umbilicus into crescent shape
high risk of incarceration/strangulation
surgical repair should be done ASAP
Acute abdomen
rapid onset of severe symptoms of abdominal pathology e.g. severe abdo pain lasting ≤5 days
Commonest causes of acute abdomen
non specific abdo pain renal colic biliary colic cholecystitis appendicitis diverticulitis
Assessment/management of acute abdomen
pt NBM IV fluids, analgesia and O2 as needed NG tube FBC, U&Es, LFTs, ABG, Ca2+, coagulation, amylase, glucose, group&save pregnancy test urinalysis AXR, CXR, USS & CT
Laparoscopy can be diagnostic & therapeutic
Gastrointestinal perforation
full thickness loss of bowel wall integrity that results in perforation peritonitis
Aetiology of Gastrointestinal perforation
perforated duodenal ulcer (most common) IBD diverticulitis acute appendicitis toxic megacolon foreign body ingestion
Presentation of Gastrointestinal perforation
sudden onset abdo pain (stabbing & intense)
sudden onset abdo distension
nausea, vomiting, constipation
fever, tachycardia, tachypnoea, hypotension
loss of liver dullness on percussion
signs of peritonitis
Investigations for Gastrointestinal perforation
Its a surgical emergency and investigations should not delay explorative laparotomy if clinic features are present
ABG (lactic acidosis), FBC (↑WCC)
AXR (free air under diaphragm)
USS (enhanced peritoneal stripe sign, air artefacts)
Management of Gastrointestinal perforation
NBM (bowel rest) IV Abx IV fluids (if needed) NG tube with free drainage urgent explorative laparotomy
Peritonitis
inflammation of the peritoneum caused by bacterial infection from a surgically treatable intra-abdominal source
Aetiology of peritonitis
- perforation of intra-abdominal viscera
- appendicitis/diverticulitis/pancreatitis (translocation of bacteria from abdominal organs)
- trauma (penetrating trauma)
- anastomotic leak
Presentation of peritonitis
abdo pain & tenderness
peritoneal signs (local/diffuse rigidity, rebound tenderness, guarding)
nausea, vomiting, ileus
shock/sepsis (hypotension, tachycardia tachypnoea, fever)
NB lack of improvement/worsening of symptoms in suspected SBP after ABx indicated peritonitis
Investigations for peritonitis
peritoneal fluid analysis (↑WCC, culture +ve, protein >1g/dL)
CT contrast of abdo/pelvis
AXR
Management of peritonitis
IV broad spectrum Abx
surgical consult for possible explorative laparotomy + lavage
Stomas
bring lumen or visceral contents through an orifice in the skin, most commonly with bowel
Features of a healthy stoma
should be red & moist
no separation between mucocutaneous edge & skin
no erythema, rash, ulceration or inflammation of surrounding skin
Ileostomy
Located in RIF
spouted
outputting liquid
Colostomy
location varies but usually L side of abdomen
flush with skin
outputting solids
Urostomy
connection between bladder & abdominal wall
output is urine
Stoma appearance
Small bowel stomas:
tend to be spouted so their irritant contents are not in contact with the skin
Colonic stomas:
can be flush with skin
Wernickes encephalopathy & Wernicke-Korsakoff syndrome
a spectrum of disease due to thiamine deficiency usually related to alcohol abuse,
increasing incidence recently
alcohol related brain damaged accounts for ~10-25% of all dementia
Wernickes encephalopathy
an acute but reversible condition
classic triad of Confusion, Ataxia, Opthalmoplegia/nystagmus
other features include perisperhal sensory neuropathy, autonomic dysfunction & ↓GCS
if untreated can progress to Wernicke-Korsakoff syndrome
Classic triad of Wernickes encephalopathy
Confusion
Ataxia
Opthalmoplegia/nystagmus
Wernicke-Korsakoff syndrome
chronic condition that is irreversible
presents with features of Wernickes (Confusion, Ataxia, Opthalmoplegia/nystagmus) plus retrograde & anterograde amnesia, personality change, confabulation, disorientation & hallucinations
Investigations for Wernickes encephalopathy & Wernicke-Korsakoff syndrome
usually clinical diagnosis
Thiamine levels (↓) FBC (macrocytic anaemia), U&Es, LFTs, glucose, MRI/CT head
Management of Wernickes encephalopathy & Wernicke-Korsakoff syndrome
IV high dose thiamine/Vit B (Pabrinex) if Wernicke’s suspected
long term oral Vit B/thiamine supplementation
alcohol abstinence
consider supplementing folate, Vit B6, Vit B12 as well
Clostridium difficile associated disease
infection of the colon by bacteria clostridium difficile (gram +ve bacillus) leading to a syndrome known as pseudomembranous colitis
Presentation of C. Diff
symptoms start 5-10 days after Abx therapy or during course of Abx
watery diarrhoea ±blood/mucous
abdominal cramps
fever
nausea
Investigations of C. Diff
FBC (↑WCC often >15x10^9/L)
U&Es (↓K+)
ABG (↓pH, ↑lactate)
Stool MC&S (detecting C. Diff toxin)
NB to diagnose C. diff the C. diff toxin must be present, if C. Diff antigen present this only means there was a past infection
Management of 1st episode of C. Diff
1st line: oral vancomycin for 10days
2nd line: oral fidaxomicin
3rd line: or vancomycin + IV metronidazole
Management of Recurrent episodes of C. Diff
if within 12 weeks of symptom resolution of previous c. diff infection = oral fidaxomicin
if >12 weeks after symptom resolution of previous c. diff infection = oral vancomycin/fidaxomicin
Aetiology of C. diff infection
often associated with Abx use especially clindamycin, cephalosporins and metronidazole
often hospital acquired
General C. Diff management
Abx (usually vancomycin or fidaxomicin)
report to PHE (if stool C. diff toxin +ve)
stop causative Abx
avoid opiates & loperamide (slow peristalsis and hence toxin is retained)
Coeliacs disease
a systemic autoimmune disease triggered by dietary gluten peptides
associated with HLA-DQ2 & HLA-DQ8 as well as other autoimmune disease
affects ~1% of population
Presentation of coeliacs disease
chronic/recurring diarrhoea & bloating
failure to thrive/faltering growth (in children)
persistent/unexplained GI symptoms e.g. N&V
prolonged fatigue
recurrent abdo pain/cramping/distension
malabsorption (e.g. IDA, folate deficiency)
dermatitis herpetiformis (pruritic papulovesicular rash occurring symmetrically over extensor surfaces)
weight loss
Investigations for coeliacs disease
Total IgA (if ↓ other tests gives false negative) Tissue transglutaminase (tTG) antibodies (+ve) endoscopic biopsy (villous atrophy, crypt hyperplasia, intra-epithelial lymphocytes)
endomysial antibodies & antigladin antibodies (not as common as tTG)
NB if pt is on gluten free diet already they should restart gluten for minimum 6 weeks before investigations
Management of coeliacs disease
gluten free diet (i.e. avoid barely/wheat/rye/oats)
Achalasia
failure of lower oesophageal sphincter to relax
usually presents in middle age as dysphagia to both liquids & solids, regurgitation of food, retrosternal pain, heartburn
investigated by oesophageal manometry (↑ sphincter tone), barium swallow (dilated oesophagus & birds beak sign), CXR
Managed with heller cardiomyomotomy or pneumatic balloon dilatation (if not fit for surgery)
Oesophageal strictures
if benign then usually secondary to persistent GORD or post-op
presents with longstanding history of progressive dysphagia to solid food
diagnosed via barium swallow & endoscopy + biopsy
treated with pneumatic ballon dilatation
NB if malignant structure then needs to be surgically excised
Pharyngeal pouch (Zenkers diverticulum)
a posteromedial diverticulum through Kilians
5:1 male:female ration, usually seen age >70yrs
presents with dysphagia, halitosis, regurgitation, aspiration, chronic cough, neck lump (gurgles on palpation)
diagnosed with barium swallow
treated with surgery, usually endoscopically
NB endoscopy should be avoided as this can perforate the lesion.
