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Year 3 > General surgery, Gastro and hepatology > Flashcards

General surgery, Gastro and hepatology Flashcards

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1
Q

Appendicitis

A

acute inflammation of the vermiform appendix usually due to obstruction of the appendiceal lumen

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2
Q

Epidemiology of appendicitis

A

Most common cause of acute abdomen in children & adults

usually presents age 10-20yrs

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3
Q

Most common cause of acute abdomen

A

Appendicitis

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4
Q

Presentation of appendicitis

A

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

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5
Q

Investigations for appendicitis

A

essentially a clinical diagnosis

FBC (↑ WCC, neutrophilia)
Pregnancy tests in females
CRP (↑)
USS or CT ± contrast

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6
Q

Management of appendicitis

A

appendectomy
-laparoscopic = 1st line

prophylactic Abx
analgesia

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7
Q

Complications of appendicitis

A 
perforation (~20%)
appendix abscess (after untreated perforation)
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8
Q

Aetiology of acute pancreatitis

A

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
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9
Q

Most common causes of acute pancreatitis

A

biliary pancreatitis (i.e. after gallstones)
alcohol induced
post ERCP, steroids, trauma

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10
Q

Presentation of acute pancreatitis

A 
constant severe epigastric pain radiating to back
 -worse after meals
 -better when leaning forward
N&V
jaundice
shock (hypotension, tachycardia)
dyspnoea
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11
Q

Investigations for acute pancreatitis

A

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

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12
Q

Glasgow score use

A

used for acute pancreatitis as a prognostic tool

alternatives include the RANSON score and the APACHE II score

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13
Q

Glasgow score for acute pancreatitis

A 
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
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14
Q

Poor prognostic indicators for acute pancreatitis

A 
age > 55 years
hypocalcaemia
hyperglycaemia
hypoxia
neutrophilia
elevated LDH and AST
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15
Q

Management of acute pancreatitis

A 
aggressive IV fluid therapy
Nil by mouth
NG tube feeding
analgesia
consider Abx if severe
Early cholecystectomy/ERCP if related to gallstones
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16
Q

Chronic pancreatitis

A

caused by progressive inflammation & irreversible damage to the structure and exocrine/endocrine functions of the pancreas

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17
Q

Aetiology of chronic pancreatitis

A

~80% due to long term heavy chronic alcohol misuse

others: cystic fibrosis, heamachromatosis, ductal obstruction

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18
Q

Epidemiology of chronic pancreatitis

A

average pt is aged 40 yrs

4:1 male: female ratio

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19
Q

Presentation of chronic pancreatitis

A 
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
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20
Q

Investigations for chronic pancreatitis

A

AXR (pancreatic calcification)
CT (more sensitive for calcifications)
FBCs/U&Es/creatinine/LFTs/Ca2+/glucose
amylase (is normal)

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21
Q

Management of chronic pancreatitis

A 
analgesia (often requires opioids)
pancreatic enzyme replacement e.g. CREON
abstinence from alcohol/smoking/drugs
supplements such as Vit ADEK
surgery if intractable pain
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22
Q

Diverticular disease

A

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)

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23
Q

Aetiology of diverticular disease

A

develop due to chronic elevations of intraluminal pressure e.g. due to constipation & the age related weakening of connective tissue

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24
Q

Risk factors diverticular disease

A

age >50 yrs
low fibre diet
obesity

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25
Presentation of Diverticulosis
non specific abdo pain/discomfort chronic constipation bloating
26
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 ```
27
Presentation of diverticular haemorrhage
painless abrupt frank PR bleeding
28
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 ```
29
Management of diverticular disease
↑ dietary fibre intake & ensure adequate fluid intake analgesia ABx for diverticulitis surgery if perforation/uncontrolled sepsis/fistula
30
Complications of diverticular disease
``` fistulas perforation leading to peritonitis abscess formation haemorrhage intestinal obstruction ```
31
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 ```
32
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
33
Presentation of Hep A
Flu like prodrome (fevers, malaise, myalgia) RUQ pain tender hepatomegaly jaundice ± pruritus/pale stools/dark urine
34
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)
35
Investigations for acute viral hepatitis
``` ALT ↑ AST ↑ ALP ↑ gamma-GT ↑ bilirubin ↑ ```
36
Management of Hep A
supportive management avoid alcohol avoid food handling avoid unprotected intercourse
37
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
38
Hepatitis B (Hep B)
most common cause of hepatitis world wide | transmitted sexually, parenterally or perinatally
39
Acute presentation of Hep B
acute illness often sub clinical or presents as flu like illness (similar to Hep A)
40
Chronic presentation of Hep B
``` chronic disease (if HbsAg +ve for >6 months) fatigue, RUQ pain ```
41
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)
42
Prevention of Hep B
vaccination on routine childhood immunisation schedule given at 2,3 and 4 months
43
Complications of Hep B
↑ risk of hepatocellular carcinoma (HCC) | chronic hepatitis
44
Hepatits C (Hep C)
transmitted parenterally e.g. IVDU/needlestick | ↑ cases in UK
45
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 ```
46
Investigations for Hep C
LFTs (↑ AST/ALT/ALP/GGT/bilirubin) Hep C antibodies (+ve in immunocompetent pts) HCV RNA (+ve)
47
Treatment for Hep C
Acute: active monitoring or interferon to ↓ risk of chronic HCV Chronic: combination of protease inhibitors ± ribavirin
48
Viral hepatitis unable to vaccinated against
Hep C has no vaccine currently available
49
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
50
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
51
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
52
Risk factors for liver cirrhosis
``` excess alcohol consumption Hep B/C infection obesity IVDU unprotected sexual intercourse ```
53
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
54
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
55
Classification of cirrhosis
Child-Pugh-Turcotte system
56
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)
57
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
58
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
59
Presentation of oesophageal varices
``` generally asymptomatic unless haemorrhaging haematemesis abdo pain malaena dysphagia/odynophagia pallor shock (hypotension, tachycardia, ↓ GCS) ```
60
Investigations for oesophageal varices
``` Endoscopy (OGD) -shows dilated veins -also therapeutic U&Es (↑ Urea) FBC, group & screen, LFTs U&Es (↑ Urea) ```
61
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
62
Prophylaxis of oesophageal varices
Propanolol | endoscopic vatical band ligation + PPI cover
63
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
64
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)
65
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)
66
Management of portal hypertension
beta blockers ± nitrates (↓ pressure) salt restriction & diuretics Transjugular intrahepatice portosystemic shunt (TIPSS)\ treat underlying cause or liver transplant
67
complications of Transjugular intrahepatice portosystemic shunt (TIPSS)
exacerbation of hepatic encephalopathy is a common complication
68
Ascites
pathological collection of fluid in the peritoneal cavity on clinical examination ~1500ml detectable on USS can detect volumes ≤500ml
69
Aetiology of ascites
``` ~75% = cirrhosis ~15% = malignancy e.g. meigs syndrome with ovarian cancer or GI tract malignancy ``` others: Heart failure, nephrotic syndrome
70
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
71
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)
72
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
73
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 ```
74
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
75
Aetiology of Spontaneous bacterial peritonitis (SBP)
most commonly E. Coli | otherwise Klebsiella
76
Presentation of Spontaneous bacterial peritonitis (SBP)
``` fever ascites abdo pain naseau & vomiting constipation/diarrhoea ```
77
Investigations for Spontaneous bacterial peritonitis (SBP)
``` ascitic tap -neutrophil count >250 cells/mm3 -ascitic fluid culture FBC blood cultures ```
78
Management of Spontaneous bacterial peritonitis (SBP)
empirical Abx (generally IV) -1st line: IV cefotaxime -2nd line: IV ceftriaxone/ciprofloxacin consider human albumin solution
79
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
80
Presentation of Hepatorenal syndorme (HRS)
jaundice ascites features of liver failure peripheral oedema
81
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
82
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
83
Treatment of Hepatorenal syndorme (HRS)
splanchnic vasoconstrictors e.g. terlipressin human album solution treat precipitating infection TIPSS
84
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
85
precipitating events for hepatic encephalopathy
``` transjugular intrahepatic portosystemic shunting (TIPSS) infections e.g. SBP renal failure constipation GI bleed ```
86
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
87
Grading of hepatic encephalopathy
I: irritability & sleep disturbances II: confusion & inappropriate behaviour III: incoherent, restless, somnolent but rousable, amnesia, disorientation IV: coma
88
Management of hepatic encephalopathy
reducing gut nitrogen load 1st line : lactulose + rifamixin (sedentary prophylaxis) 2nd line enemas
89
Prophylaxis of hepatic encephalopathy
Rifamixin reduces recurrences
90
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
91
Portopulmonary hypertension
unexplained pulmonary hypertension in association with portal hypertension often asymptomatic requires echo & right heart catheterisation treatment is liver transplant
92
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)
93
Aetiology of Hepatocellular carcinoma (HCC)
chronic Hepatitis B or C infections (most common cause) alcoholic liver disease others: haemochromatosis, primary biliary cirrhosis
94
Epidemiology of Hepatocellular carcinoma (HCC)
more common in men (~4x) | usually seen age 65-70 yrs
95
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 ```
96
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)
97
Investigations for Hepatocellular carcinoma (HCC)
``` Serum AFP (↑) LFTs, FBC, Clotting liver USS (best initial investigation) contrast enhanced CT/MRI abdo liver biopsy ```
98
Tumour marker for Hepatocellular carcinoma (HCC)
Serum Alpha fetoprotein (AFP)
99
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
100
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
101
Risk factors for Non alcoholic fatty liver disease (NAFLD)
``` obesity T2DM hyperlipidaemia jejunoileal bypass sudden weight loss/starvation metabolic syndrome HTN total parenteral nutrition ```
102
Presentation of Non alcoholic fatty liver disease (NAFLD)
``` often asymptomatic hepatomegaly obesity fatigue features of cirrhosis ```
103
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
104
Management of Non alcoholic fatty liver disease (NAFLD)
lifestyle changes (diet &exercise) weight loss monitoring of disease
105
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
106
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
107
Genetics of wilson's disease
autosomal recessive mutations of ATP7b gene
108
Epidemiology of Wilson's disease
RARE condition onset usually age 10-25yrs usually goes undiagnosed until combination of hepatitis, dementia & Parkinsonism causes clinical suspicion
109
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
110
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) ```
111
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)
112
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
113
genetics of Haemochromatosis
autosomal recessive mutation of the HFE gene
114
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)
115
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
116
Management of Haemochromatosis
1st line: phlebotomy/venesection 2nd line: desferrioxamine Liver transplant in end stage liver disease
117
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
118
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
119
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
120
Risk factors for gallstones
``` ↑age FH of gallstones sudden weight loss diabetes oral contraception pregnancy female gender ```
121
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
122
Investigations for gallstones
USS of RUQ (demonstrates stones) -if -ve but high index of suspicion then repeat ERCP or CT
123
Management of gallstones
expectant management if asymptomatic ERCP (to remove stones) elective laparoscopic cholecystectomy
124
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)
125
Risk factors for Acute cholecystitis
``` gallstones female gender ↑age obesity pregnancy Crohns disease hyperlipidaemia ```
126
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
127
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
128
Management of Acute cholecystitis
``` IV Abx analgesia e.g. morphine early laparoscopic cholecystectomy -within 1 week of diagnosis -gold standard ```
129
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
130
Presentation of Acute/ascending cholangitis
Charcots triad: 1. RUQ pain (maybe poorly localised abdo pain in elderly) 2. Fever 3. Jaundice Raynauds pentad 1. RUQ pain (maybe poorly localised abdo pain in elderly) 2. Fever 3. Jaundice 4. hypotension (septic shock) 5. confusion
131
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 ```
132
management of Acute/ascending cholangitis
IV ABx & IV fluids analgesia endoscopic retrograde cholangipancreatography (ERCP) -after 24-48h to relieve any obstruction
133
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
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Conditions associated with Primary biliary cholangitis (PBC)
Sjogrens syndrome (up to 80% of pts) Rheumatoid arthritis systemic sclerosis thyroid disease
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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) ```
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Investigations for Primary biliary cholangitis (PBC)
``` LFTs (↑ gamma-GT, ↑ALP, ↑bilirubin) ESR (↑) IgM (↑) anti-mitochondrial antibodies (AMA) M2 (+ve) abdo USS MRI cholangiopancreatography (MRCP) ```
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Management of Primary biliary cholangitis (PBC)
1st line: ursodeoxycholic acid cholestyramine for prurits Vit ADEK supplements
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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
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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
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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
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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)
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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) ```
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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
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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
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Risk factors for Crohn's disease
Family history smoking (smokers tend to have more aggressive disease) HLA-B27
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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
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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 ```
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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 ```
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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
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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
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Maintaining remission in Crohn's disease
1st line: azathioprine/mercaptopurine (assess TPMT activity before starting) 2nd line: methotrexate
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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
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Ulcerative colitis (UC) epidemiology
most common form of IBD | peak incidence age 15-25 yrs
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Risk factors for Ulcerative colitis (UC)
HLA-B27 white ehtnicity FH of IBD
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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
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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
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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)
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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
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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
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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
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Epidemiology for Irritable bowel syndrome (IBS)
affects 10-20% of population more common in women most prevalent in ages 20-30yrs
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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
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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
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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
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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
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Epidemiology of Gastro-oesophageal reflux disease (GORD)
2-3x more common men
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Epidemiology of Gastro-oesophageal reflux disease (GORD)
2-3x more common men
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Risk factors for Gastro-oesophageal reflux disease (GORD)
``` smoking stress obesity pregnancy hiatus hernia caffeine alcohol ```
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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 ```
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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
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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
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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
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Epidemiology of Barretts oesophagus
seen in ~5% of pts with GORD more common in men more common in caucasians
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Presentation of Barretts oesophagus
often asymptomatic usually GORD symptoms i.e. reflux, heartburn etc symptoms of oesophageal stricture e.g. dysphagia
175
Risk factors for Barretts oesophagus
``` GORD male gender smoking central obesity hiatus hernia ```
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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
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Management of Barretts oesophagus
endoscopic surveillance with biopsy (every 3-5 years) high dose PPI if dysplasia identified - endoscopic mucosal resection - radio frequency ablation
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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
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Risk factors for oesophageal cancer
``` smoking GORD/Barretts oesophagus (for adenocarcinoma) strictures (for SCC) obesity (for adenocarcinoma) Plummer Vinson syndrome (for SCC) ```
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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
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Presentation of oesophageal cancer
``` dysphagia vomiting weight loss anorexia odynophagia hoarseness retrosternal pain ```
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2 week wait criteria for suspect oesophageal cancer
unexplained dysphagia at any age age >55 + weight loss and upper abdo pain/reflux/dyspepsia
183
Investigations for oesophageal cancer
OGD with biopsy CT chest/abdo/pelvis FBC, U&Es, LFTs, CRP
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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
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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
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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
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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
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Peptic ulcer disease (PUD)
the presence of one or more ulcerative lesions in the stomach or duodenum break in mucosal lining should be >5mm
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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)
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Conditions associated with H. Pylori infection
Peptic ulcer disease (PUD) | Gastric MALT lymphoma (good prognosis)
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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
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Presentation of gastric ulcer
epigastric pain aggravated by eating
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Presentation of duodenal ulcer
epigastric pain when hungry | pain is relieved by eating
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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
195
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
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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
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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
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Aetiology of Upper GI bleed
``` peptic ulcer disease (~25%) oesophagi's gastritis/erosions varices malignancy Mallory-weiss tear ``` ~20% no aetiology is found
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Presentation of Upper GI bleed
haematemesis malaena signs of shock (hypotension, tachycardia, tachypnoea)
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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
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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
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Post-endoscopy scoring system for Upper GI bleed
Rockall score - used post endoscopy - identifies risk of adverse outcomes
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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
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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
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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
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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)
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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
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Prophylaxis of variceal bleeding
Propanolol | Endoscopic band ligation with PPI cover
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Lower GI bleed
a wide clinical spectrum from small bleeding to major haemorrhage incidence increases with age
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Aetiology of Lower GI bleed
``` Diverticular disease (15-40%) Meckels diverticulum colonic angiodysplasisa (common in older people) ischaemic colitis colonic cancer haemorrhoidal bleeding ```
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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)
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Investigations for Lower GI bleed
colonoscopy after bowel prep (OGD if colonoscopy -ve) PR examination CT angiography FBC, coagulation, U&Es
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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
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Pancreatic cancer
generally refers to primary pancreatic ductal adenocarcinoma which accounts for ~85% of all pancreatic neoplasms
215
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
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pathognomonic presentation of pancreatic cancer
Painless jaundice is pancreatic cancer until proven otherwise
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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
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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) ```
219
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
220
Management of pancreatitis
Whipples resection (pancreaticoduodenectomy) + adjuvant chemo Palliative chemo & radiotherapy, ERCP + stent placement NB only ~20% suitable for surgery at diagnosis
221
Tumour marker for pancreatic cancer
Ca 19-9
222
Common metastasis sites of pancreatic cancer
Liver Peritoneum abdominal viscera lungs
223
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
224
Risk factors for Gastric cancer
``` H. Pylori male gender smoking diet (high in salt) atrophic gastritis FH of gastric cancer ```
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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)
226
Investigations for Gastric cancer
endoscopy with biopsy -may show signet ring cells CT chest/abdo/pelvis FBC, LFTs, U&Es
227
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
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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
229
Most common site of metastasis for colorectal cancer
Liver other sites e.g. brain/lungs/bones are uncommon if liver mets not present
230
Most common site of Colorectal cancer
Rectum
231
Risk factors for Colorectal cancer
``` FH of colorectal neoplasia IBD Polyposis syndromes HNPCC (lynch syndrome) obesity smoking alcohol abuse diabetes ```
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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
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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
234
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
235
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
236
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
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Presentation of Left sided colorectal cancer
colicky pain, rectal bleeding, bowel obstruction, tenesmus, LIF mass, early change in bowel habit, blood in stool
238
Presentation of Rectal cancer
haematochezia, ↓ stool caliber (pencil shaped stools), rectal pain, tenesmus, flatulence, faecal incontinence
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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
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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
241
Investigations for colonic polyps
colonoscopy + biopsy double contrats barium enema CT colonography FIT testing, Hb
242
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
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Hereditary polyposis syndromes
``` Familial adenomatous polyposis MYH associated polyposis Peutz-Jeghers syndrome Juvenile polyposis Cowden sydrome ```
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Hereditary polyposis syndromes
``` Familial adenomatous polyposis MYH associated polyposis Peutz-Jeghers syndrome Juvenile polyposis Cowden sydrome ```
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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
246
MYH associated polyposis
autosomal recessive mutation of MUTYH gene <100 polyps seen on endoscopy treated with prophylactic proctocolectomy with ill-pouch-anal anastomosis
247
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
248
Juvenile polyposis
onset within first decade of life presents with Gi bleeding & anaemia
249
Cowden syndrome
autosomal dominant mutation of PTEN gene presents with multiple GI polyps and skin manifestations (hyperkeratosis & papules) associated with breast cancer & thyroid disorders
250
Haemorrhoids (piles)
Haemorrhoidal cushions are normal anatomical structures within the anal canal, which may enlarge & protrude outdid the anal canal
251
Types of Haemorrhoids
internal (originate above dentate line) external (originate below dentate line)
252
Risk factors for Haemorrhoids
excessive straining e.g. chronic constipation extended periods of sitting pregnancy low fibre diet
253
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
254
Investigation for Haemorrhoids
PR examination | shows tenderness, masses and bleeding
255
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
256
Small bowel obstruction
a mechanical disruption of the potency of the GI tract which is a medical emergency requiring early diagnosis & intervention
257
Risk factors for Small bowel obstruction
previous abdominal surgery hernias foreign body ingestion intestinal malignancy
258
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 ```
259
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
260
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 ```
261
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
262
Large bowel obstructions
complete or partial mechanical interruption of flow of intestinal contents surgical emergency
263
Aetiology of Large bowel obstruction
~60% colorectal malignancy ~20% diverticular strictures ~5% volvulus
264
Risk factors for Large bowel obstruction
``` colorectal adenomas/polyps current/previous malignancy IBD diverticular disease current/previous hernia previous abdo surgery ```
265
Presentation of Large bowel obstruction
``` intermitten abdo pain significant abdo distension nausea & vomiting total constipation high pitched bowel sounds tympanic percussion empty rectum ```
266
Investigations for Large bowel obstruction
AXR (1st line) CT abdo/pelvis (dilation, shows underlying cause) FBC, U&Es, group & screen
267
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
268
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
269
Type of volvulus
Sigmoid volvulus: -associated with older pts & chronic constipation Caecal volvulus: -tends to be younger pts
270
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)
271
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
272
Management of volvulus
Sigmoid: rigid sigmoidoscopy with recatl tube insertion Caecal: right hemicolectomy often needed
273
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
274
Presentation of Toxic megacolon
bloody diarrhoea, vomiting abdo distension & pain sepsis (fever, hypotension, tachycardia, dehydration)
275
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
276
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
277
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
278
Risk factors of Abdominal aortic aneurysm (AAA)
``` ↑age smoking* atherosclerosis hypercholesterolaemia FH of AAA hypertension ```
279
Presentation of unruptered Abdominal aortic aneurysm (AAA)
generally asymptomatic (i.e. incidental finding) back pain pulsate abdominal swelling bruit on auscultation
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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%
281
Investigations for Abdominal aortic aneurysm (AAA)
abdo USS (aorta diamete >3cm) CT angiography (especially if pt symptomatic)
282
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
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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
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Epidemiology of Abdominal aortic aneurysm (AAA)
more common elderly men usually aged >60yrs NB rupture of AAA is more common in women
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Management of ruptured Abdominal aortic aneurysm (AAA)
resuscitation & blood transfusion end-vascular aneurysm repair (EVAR) or open surgical repair within 90 min
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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
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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
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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
289
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
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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
291
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
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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
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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
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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
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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
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Management of inguinal hernia
surgical repair of hernia
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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
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Femoral hernias
protrusion of abdominal viscera into the femoral canal accounts for ~5% of abdominal hernias more common in women, especially if multiparous
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Presentation of femoral hernia
lump in groin - lateral & inferior to pubic tubercle - swells on coughing/straining - typically non reducible
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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
301
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
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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
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Acute abdomen
rapid onset of severe symptoms of abdominal pathology e.g. severe abdo pain lasting ≤5 days
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Commonest causes of acute abdomen
``` non specific abdo pain renal colic biliary colic cholecystitis appendicitis diverticulitis ```
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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
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Gastrointestinal perforation
full thickness loss of bowel wall integrity that results in perforation peritonitis
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Aetiology of Gastrointestinal perforation
``` perforated duodenal ulcer (most common) IBD diverticulitis acute appendicitis toxic megacolon foreign body ingestion ```
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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
309
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)
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Management of Gastrointestinal perforation
``` NBM (bowel rest) IV Abx IV fluids (if needed) NG tube with free drainage urgent explorative laparotomy ```
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Peritonitis
inflammation of the peritoneum caused by bacterial infection from a surgically treatable intra-abdominal source
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Aetiology of peritonitis
- perforation of intra-abdominal viscera - appendicitis/diverticulitis/pancreatitis (translocation of bacteria from abdominal organs) - trauma (penetrating trauma) - anastomotic leak
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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
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Investigations for peritonitis
peritoneal fluid analysis (↑WCC, culture +ve, protein >1g/dL) CT contrast of abdo/pelvis AXR
315
Management of peritonitis
IV broad spectrum Abx | surgical consult for possible explorative laparotomy + lavage
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Stomas
bring lumen or visceral contents through an orifice in the skin, most commonly with bowel
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Features of a healthy stoma
should be red & moist no separation between mucocutaneous edge & skin no erythema, rash, ulceration or inflammation of surrounding skin
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Ileostomy
Located in RIF spouted outputting liquid
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Colostomy
location varies but usually L side of abdomen flush with skin outputting solids
320
Urostomy
connection between bladder & abdominal wall | output is urine
321
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
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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
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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
324
Classic triad of Wernickes encephalopathy
Confusion Ataxia Opthalmoplegia/nystagmus
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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
326
Investigations for Wernickes encephalopathy & Wernicke-Korsakoff syndrome
usually clinical diagnosis ``` Thiamine levels (↓) FBC (macrocytic anaemia), U&Es, LFTs, glucose, MRI/CT head ```
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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
328
Clostridium difficile associated disease
infection of the colon by bacteria clostridium difficile (gram +ve bacillus) leading to a syndrome known as pseudomembranous colitis
329
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
330
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
331
Management of 1st episode of C. Diff
1st line: oral vancomycin for 10days 2nd line: oral fidaxomicin 3rd line: or vancomycin + IV metronidazole
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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
333
Aetiology of C. diff infection
often associated with Abx use especially clindamycin, cephalosporins and metronidazole often hospital acquired
334
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)
335
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
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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
337
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
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Management of coeliacs disease
gluten free diet (i.e. avoid barely/wheat/rye/oats)
339
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)
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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
341
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.

Year 3 (6 decks)

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