gastro 4 Flashcards
(108 cards)
1
Q
what causes splenic rupture?
A
usually secondary to abdominal trauma
a minority of cases are iatrogenic or secondary due to splenomegaly from haematological malignancy or infective causes
2
Q
what are the clinical features of spLenic rupture?
A
abdominal pain
hypovolemic shock
LUQ tenderness
radiating left shoulder pain caused by free blood irritating the diaphragm
3
Q
what investigations would you perform for splenic rupture?
A
immediate laparotomy if they are hemodynamically unstable
if they are hemodynamically stable - urgent CT chest abdo pelvis with IV contrast
4
Q
what scale is used for splenic injury ?
A
The American Association for the Surgery of Trauma (AAST) splenic injury scale is the most commonly used system for grading splenic trauma.
5
Q
what is splenic infarct?
A
A splenic infarct is caused by occlusion of the splenic artery or one of its branches, resulting in tissue necrosis.
As the spleen is supplied by the splenic artery (from the coeliac axis) and the short gastric arteries (from left gastroepiploic artery), infarction is often not complete due to collateral circulation.
6
Q
what can cause splenic infarct?
A
Haematological disorders* such as lymphoma, myelofibrosis, Sickle Cell Disease, Chronic Myeloid Leukaemia, Polycythaemia Rubra Vera, or hypercoagulable states
Embolic disorders such as endocarditis, atrial fibrillation, infected aneurysm grafts, or post-MI mural thrombus
other causes include vasculitis, trauma, collagen tissue disease
7
Q
what are the clinical features of splenic infarct?
A
LUQ abdominal pain which may radiate to the left shoulder
other symptoms include - fever, nausea, vomiting, pleuritic chest pain
many people will be completely asymptomatic
8
Q
what investigations would you perform for splenic infarct?
A
CT abdomen with IV contrast
routine bloods
9
Q
how is splenic infarct managed?
A
analgesia
hydration
treat underlying condition
10
Q
what is bile acid malabsorption?
A
Bile-acid malabsorption is a cause of chronic diarrhoea. This may be primary, due to excessive production of bile acid, or secondary to an underlying gastrointestinal disorder causing reduced bile acid absorption. It can lead to steatorrhoea and vitamin A, D, E, K malabsorption.
11
Q
what investigations would you perform for bile-acid malabsorption?
A
the test of choice is SeHCAT
nuclear medicine test using a gamma-emitting selenium molecule in selenium homocholic acid taurine or tauroselcholic acid (SeHCAT)
scans are done 7 days apart to assess the retention/loss of radiolabelled 75SeHCAT
12
Q
how do you manage bile acid malabsorption?
A
bile acid sequestrants e.g. cholestyramine
13
Q
what is budd-chiari syndorme?
A
aka hepatic vein thrombosis
s usually seen in the context of underlying haematological disease or another procoagulant condition.
14
Q
what are the causes of budd-chiari syndrome?
A
polycythaemia rubra vera
thrombophilia: activated protein C resistance, antithrombin III deficiency, protein C & S deficiencies
pregnancy
combined oral contraceptive pill: accounts for around 20% of cases
15
Q
what are the features of budd-chiari syndrome?
A
The features are classically a triad of:
abdominal pain: sudden onset, severe
ascites → abdominal distension
tender hepatomegaly
16
Q
what investigations would you perform for budd-chiari syndrome?
A
ultrasound with Doppler flow studies is very sensitive and should be the initial radiological investigation
17
Q
what is gilbert’s syndrome?
A
Gilbert’s syndrome is an autosomal recessive condition of defective bilirubin conjugation due to a deficiency of UDP glucuronosyltransferase.
18
Q
what are the features of Gilbert’s syndrome?
A
unconjugated hyperbilirubinaemia (i.e. not in urine) jaundice may only be seen during an intercurrent illness, exercise or fasting
19
Q
what are the investigations and management of Gilbert’s syndrome?
A
investigation: rise in bilirubin following prolonged fasting or IV nicotinic acid
no treatment required
20
Q
what is Meckel’s diverticulum?
A
Meckel’s diverticulum is a congenital diverticulum of the small intestine. It is a remnant of the omphalomesenteric duct (also called the vitellointestinal duct) and contains ectopic ileal, gastric or pancreatic mucosa
21
Q
what is the rule of 2’s in Meckel’s diverticulum?
A
occurs in 2% of the population
is 2 feet from the ileocaecal valve
is 2 inches long
22
Q
how does meckel’s diverticulum present?
A
usually asymptomatic abdominal pain which mimics appendicitis rectal bleeding (common cause of painless massive GI bleed requiring transfusion in children between the ages of 1 and 2) intestinal obstruction secondary to a volvulus
23
Q
what investigations would you perform for suspected meckel’s diverticulum ?
A
FBC technetium-99 pertechnetate scan (meckel's scan) plain abdo xray CT scan USS
24
Q
How is Meckel’s diverticulum managed?
A
if incidental finding - no treatment requires
if symptomatic - excision of the diverticulum and opposing region of ileum
25
what can cause acute liver failure?
paracetamol overdose
alcohol
viral hepatitis (usually A or B)
acute fatty liver of pregnancy
26
what are the features of acute liver failure ?
```
jaundice
coagulopathy: raised prothrombin time
hypoalbuminaemia
hepatic encephalopathy
renal failure is common ('hepatorenal syndrome')
```
27
what tests would you perform to look at the synthetic function of the liver?
liver function tests' do not always accurately reflect the synthetic function of the liver. This is best assessed by looking at the prothrombin time and albumin level.
28
what is non alcoholic fatty liver disease?
part of the “metabolic syndrome” group of chronic health conditions relating to processing and storing energy that increase risk of heart disease, stroke and diabetes.
It is characterised by fat deposited in liver cells. These fat deposits can interfered with the functioning of the liver cells. NAFLD does not cause problems initially, however it can progress to hepatitis and cirrhosis.
29
what are the stages of non alcoholic fatty liver disease?
1. Non-alcoholic Fatty Liver Disease
1. Non-Alcoholic Steatohepatitis (NASH)
1. Fibrosis
3. Cirrhosis
30
risk factors for non-aloholic fatty liver disease?
```
Obesity
Poor diet and low activity levels
Type 2 diabetes
High cholesterol
Middle age onwards
Smoking
High blood pressure
```
31
what is a non-invasive liver screen?
Ultrasound Liver
Hepatitis B and C serology
Autoantibodies (autoimmune hepatitis, primary biliary cirrhosis and primary sclerosing cholangitis)
Immunoglobulins (autoimmune hepatitis and primary biliary cirrhosis)
Caeruloplasmin (Wilsons disease)
Alpha 1 Anti-trypsin levels (alpha 1 anti-trypsin deficiency)
Ferritin and Transferrin Saturation (hereditary haemochromatosis)
32
what investigations would you perform for non-alcoholic fatty liver?
Liver USS
Enhanced liver fibrosis blood test
fibroscan
33
how would you manage non-alcoholic fatty liver?
Weight loss
Exercise
Stop smoking
Control of diabetes, blood pressure and cholesterol
Avoid alcohol
Refer patients with liver fibrosis to a liver specialist where they may treat with vitamin E or pioglitazone.
34
what is liver failure>
Hepatic failure occurs when the liver loses the ability to regenerate or repair, so that decompensation occurs. It is marked by:
- hepatic encephalopathy
- abnormal bleeding
- ascites
- jaundice
35
how can liver failure be classified?
> Fulminant hepatic failure (FHF) occurs when the failure takes place within eight weeks of the onset of the underlying illness.
> Late-onset hepatic failure (also called subacute FHF) occurs when there has been a gap of 8-26 weeks. The difference may not immediately be obvious, as the underlying disease may have been present for a long time but undiagnosed.
> Chronic decompensated hepatic failure occurs when the latent period is over six months.
36
what are causes of liver failure?
Toxins (chronic alcohol abuse, paracetamol poisoning, illicit drugs, reye's syndrome)
Infections (viral hepatitis, adenovirus, EBV, CMV)
neoplastic (hepatocellular, metastatic carcinoma)
Metabolic (wilson's disease, alpha-1antitrypsin deficiency)
Vascular - ischaemia or veno-occlusive disease, budd-chiari syndrome
autoimmune liver disease
37
what may you find on examination of someone with liver failure?
mental state may show drowsiness and confusion
jaundice
hyperdynamic circulation with multiple organ failure may mimic septic shock
abdominal distension (ascites, hepatomegaly, splenomegaly)
cerebral oedema with increased ICP may produce papilloedema, HTN and bradycardia)
hepatic flap
hepatic encephalopathy
38
what investigations would you perform for liver failure?
```
FBC
INR
transaminases
bilirubin
ammonia
glucose
ABG
viral serolgy
test for specific condition (wilsons and paracetamol)
dopple USS
CT/MRI
head imaging
```
39
how is liver failure managed?
manage specific underlying condition
lactulose with neomycin to reduce ammonia production
mannitol may reduce raised ICP
AKI may require hemodialysis
glucose monitoring - large amounts of IV glucose may be required
Fresh-frozen plasma, platelet concentrates, antifibrinolytic drugs, prothrombin complex concentrates and recombinant activated factor VII are often used to treat or prevent abnormal bleeding .
liver transplant - may be life saving
40
what are the complications of liver failure?
infection - spontaneous peritonitis common, opportunistic pneumonia may occur
cerebral oedema and raised ICP
haemorrhage, oesophageal varacies
41
what is hepatic encecphalopathy?
Hepatic encephalopathy is defined as a spectrum of neuropsychiatric abnormalities in patients with liver failure
42
what are some common precipitants of hepatic encephalopathy?
```
Acute kidney injury.
Electrolyte imbalance.
Gastrointestinal bleeding.
Infection.
Constipation.
Sedative drugs - eg, opiates, benzodiazepines, antidepressants and antipsychotic drugs.
Diuretics.
High protein intake.
```
43
how does hepatic encephalopathy present?
```
mood disturbances (euphoria or depression)
sleep disturbance (insomnia or hypersomnia)
motor disturbance - ataxia, extrapyramidal symptoms (muscle rigidity, bradykinesia, hypokinesia, slow monotonous speech, parkinsonian like tremor)
```
44
what investigations would you perform for hepatic encephalopathy?
```
liver tests (abnormal)
serum glucose
ammonia levels
coagulation profile (elevated prothrombin time)
serum electrolytes (may have hyponatraemia or hypokalaemia)
U&E's
ABG (metabolic alkalosis)
FBC
urine toxin screen
USS of liver
head CT scan
```
45
how s hepatic encephalopathy managed?
supportive care and reversal of precipitating factors
Lactulose
rifaximin can be added to help with ammonia levels
46
what is spontaneous bacterial peritonitis?
Spontaneous bacterial peritonitis (SBP) is an infection of ascitic fluid that cannot be attributed to any intra-abdominal, ongoing inflammatory, or surgically correctable condition. It is one of the most frequently encountered bacterial infections in patients with cirrhosis.
47
what is secondary peritonitis?
This occurs when a pathological process adjacent to the peritoneum causes inflammation. Perforation of a viscus is a typical example.
48
what is localised peritonitis?
This term is used when the inflammation is in a limited area, such as adjacent to an inflamed appendix or diverticulum prior to rupture.
49
what is generalised peritonitis?
As one might suspect, this term is used when the inflammation is widespread - eg, after the rupture of a viscus.
50
what pathogens are most likely to cause spontaneous bacterial peritonitis?
```
Escherichia coli
Staphylococcus aureus
Streptococcus pneumoniae
Enterococcus faecalis
Klebsiella pneumoniae
Pseudomonas aeruginosa
```
51
how does spontaneous bacterial peritonitis present?
```
abdominal pain or tenderness
signs of ascites
fever
nausea and vomiting
diarrhoea
```
52
what investigations would you perform for spontaneous bacterial peritonitis?
FBC (leukocytosis, anaemia)
serum creatinine - may be elevated (hepatorenal syndrome may occur in patients with decompensated liver cirrhosis)
ascitic fluid appearance (hazy, cloudy, bloody), neutrophil count, gram stain and culture.
blood culture
LFTs
prothrombin/INR
53
how is spontaneous bacterial peritonitis managed?
IV Abx - cefotaxime or ceftriaxone
| if ongoing/secondary prophylaxis (antibiotic prophylaxis (ciprofloxacin) and BB (propranolol)
54
what are causes of bleeding into the abdomen?
ruptured abdominal aortic aneurysm
ruptured ectopic
bleeding gastic ulcer
trauma
55
what can cause a perforated viscus?
peptic ulceration
small or large bowel obstruction
diverticular disease
inflammatory bowel disease
56
what is the most common cause of generalised peritonitis?
perorated viscus (loss of gastrointestinal wall integrity)
57
how will generalised peritonitis present?
they will often lay completely still
they will have tachycardia and potential hypotension
rigid abdomen with percussion tenderness
involuntary guarding
reduced or absent bowel sounds
58
what is peritonism?
Peritonism (not peritonitis) refers to the localised inflammation of the peritoneum, usually due to inflammation of a viscus that then irritates the visceral (and subsequently, parietal) peritoneum.
This leads to patients stating that their abdominal pain starts in one place (irritation of the visceral peritoneum) before localising to another area* (irritation of the parietal peritoneum) or becoming generalised.
The classic example of this is acute appendicitis, with the pain migrating from the umbilical region to the right iliac fossa
59
what is an inta-abdominal abscess?
Intra-abdominal abscess (IAA), also known as intraperitoneal abscess, is an intra-abdominal collection of pus or infected material and is usually due to a localised infection inside the peritoneal cavity. It can involve any intra-abdominal organ or can be located freely within the abdominal or pelvic cavities, including in between bowel loops. IAA is almost always secondary to a pre-existing disease process, or concomitant intra-abdominal process.
60
how do intra-abdominal abscess usually present?
```
fever
abdo pain
tachycardia
change in bowel habit
nausea and vomiting
```
61
how are intra-abdominal abscess diagnosed?
WBC count
| abdominal CT
62
how are intra-abdominal abscess managed?
CT/USS guided drainage is first line for a simple abscess
| plus broad spectrum antibiotics - ticarcillin/clavulanic acid
63
what are the two main types of oesophageal cancer?
squamous cell carcinoma (middle and upper third of oesophagus - associated with smoking and excessive alcohol)
Adenocarcinoma (lower 3rd of oesophagus, arises as a consequence of barrett's oesophagus - risk factors are long standing GORD, obesity, high fat intake)
64
what are the clinical features of oesophageal cancer?
- often early stage there is a lack of well-defined symptoms
- dysphagia (Any patient with dysphagia should be assumed to have oesophageal cancer until proven otherwise)
- weight loss
- odynophagia
- hoarseness
- supraclavicular lymphadenopathy
65
what investigations would you perform for oesophageal cancer?
anyone with suspected oesophageal cancer should be offered urgent upper GI endoscopy (duodenoscopy/OGD) within 2 weeks
- Biopsy and histology
- CT chest-abdo-pelvis and PET scan to look for mets
- endoscopic USS to measure the penetration into oesophageal wall
- fine needle aspiration of palpable lymh nodes
66
how is oesophageal cancer managed?
For the majority of patients, it is surgery with or without neoadjuvant chemotherapy or chemo-radiotherapy:
Squamous cell carcinoma – SCCs of the upper oesophagus are technically difficult to operate on and definitive chemo-radiotherapy is therefore usually the treatment of choice
Adenocarcinomas – the treatment of choice is typically neoadjuvant chemotherapy or chemo-radiotherapy followed by oesophageal resection
If patients too unfit then palliative options
- stent
- radio and or chemo can be used to reduce tumour size
- nutritional support
67
what is the most standard procedure for oesophageal cancer?
Ivor-Lewis oesophagectomy
| * this biggest surgical challenge is anastomotic leak
68
what is the most common type of gastric cancer?
adenocarcinomas (>90%)
others include connective tissue, lymphoid or neuroendocrine malignancies)
69
what are the risk factors of gastric cancer?
```
male gender
H.pylori infection
increasing age
smoking
alcohol
salt in diet
positive family history
gastic adenomatous polyps
pernicious anaemia
```
70
what are the clinical features of gastric cancer?
```
dyspepsia
dysphagia
early satiety
vomiting
melena
weight loss
anaemia
epigastric mass
Troisier sign - palpable left supraclavicular node (a sign of metastatic abdo malignancy)
```
71
what investigations would you perform for gastric cancer?
Bloods - FBC and LFTs
urgent OGD
biopsy and histology - signet ring cells may be seen in gastric cancer
CLO test - for the presence of H.pylori
HER2/neu protein - this will allow for targeted monoclonal therapies if present
for staging
CT chest-abdomen and staging laparoscopy - most common staging is TNM staging
72
how is gastric cancer managed?
mainstay of treatment is surgery
they may have peri-operative chemi
Proximal gastric cancers – total gastrectomy
Distal gastric cancers (antrum or pylorus) – subtotal gastrectomy
73
what are the different types of colorectal cancer?
colorectal cancer originate from the epithelial cells lining the colon or rectum- most commonly adenocarcinoma
rarer types - lymphoma, carcinoid, sarcoma
**Most colorectal cancers develop via a progression of normal mucosa to colonic adenoma (colorectal ‘polyps’) to invasive adenocarcinoma (termed the “adenoma-carcinoma sequence”). Adenomas may be present for 10 years or more before becoming malignant and progression to adenocarcinoma occurs in approximately 10% of adenomas.
74
what genetic mutations have been found to predispose individuals to colorectal cancer?
Adenomatous polyposis coli (APC)
A tumour suppressor gene, mutation of the APC gene results in growth of adenomatous tissue; associated with Familial Adenomatous Polyposis (FAP)
Hereditary nonpolyposis colorectal cancer (HNPCC)
A DNA mismatch repair gene, mutation to HNPCC leads to defects in DNA repair; associated with Lynch syndrome
75
what are risk factors for colorectal cancer?
```
increasing age
family history
IBD
low fibre diet
high processed meat intake ]smoking
high alcohol intake
```
76
what are the clinical features of colorectal cancer?
```
change in bowel habit
rectal bleeding
weight loss
abdominal pain
iron deficiency anaemia
```
ight-sided colon cancers – abdominal pain, occult bleeding / anaemia, mass in right iliac fossa, and often present late
Left-sided colon cancers – rectal bleeding, change in bowel habit, tenesmus, mass in left iliac fossa or on PR exam
77
what investigations can be used to investigate colon cancer?
colonoscopy, endoscopy, can include biopsy or tattooing to mark for surgery (gold standard for diagnosis
CT colonography
Staging CT scan
FBC and LFTs
CEA - tumour marker for bowel cancer (not useful in screening, useful in predicting relapse of previously treated bowel cancer
78
how is colorectal cancer managed?
surgery plus neoadjuvant/adjuvant radio/chemo
- hemicolectomy
- sigmoidcolectomy
- anterior resection
Hartmann's procedure
This procedure is used in emergency bowel surgery, such as bowel obstruction or perforation. This involves a complete resection of the recto-sigmoid colon with the formation of an end colostomy and the closure of the rectal stump
79
what staging is used in colorectal cancer?
Dukes Classification
Dukes A – confined to mucosa and part of the muscle of the bowel wall
Dukes B – extending through the muscle of the bowel wall
Dukes C – lymph node involvement
Dukes D – metastatic disease
Dukes is being replaced by the TNM classification
T (tumour)
```
TX – unable to assess size
T1 – submucosal involvement
T2 – involvement of muscularis propria
T3 – involvement of the subserosa
T4 – spread directly to other tissues / peritoneum
N (nodes)
```
```
NX – unable to assess nodes
N0 – no nodal spread
N1 – spread to 1-3 nodes
N2 – spread to >3 nodes
M (metastasis)
```
M0 – no petastasis
M1 – metastasis
80
what is a covering loop ileostomy?
A temporary ileostomy created to protect a distal anastomosis
Typically left for 6-8 weeks to allow healing of the anastomosis, after which is it reversed
“Loop” refers to it being the two ends (proximal and distal) of a section of small bowel being brought out onto skin
Proximal end (the productive side) has turned inside out to form a spout to protect the surrounding skin
Usually located lower right side of abdomen
81
what screening is used for colorectal cancer?
Faecal immunochemical test - screening offered every 2 years to all men and woman aged 60 to 74 in England
82
what are the different types of anal cancer?
The majority of anal cancers are squamous cell carcinomas, arising from below the dentate line (Fig. 1). The remainder (~10%) are adenocarcinomas arise from the upper anal canal epithelium and the crypt glands.
83
risk factors for anal cancer?
```
HPV infection
increasing age
smoking
immunosuppression
Crohn's disease
```
84
what are the features of anal cancer?
```
rectal pain
rectal bleeding
anal discharge
pruritus
palpable mass
```
85
what investigations for anal cancer?
examination under anaesthetic and biopsy can be taken
CT thorax abdomen pelvis - for distant metastases
MRI pelvis
86
how is anal cancer managed?
chemo and radio
87
why does hepatocellular cancer arise?
arises as a result of a chronic inflammatory process affecting the liver
commonly due to viral hepatitis, other causes include hronic alcoholism, hereditary haemochromatosis, primary biliary cirrhosis (PBC), and aflatoxin (a toxic fungal metabolite that can be found on cereals and nuts).
88
risk factors for hepatocellular carcinoma?
```
viral hepatitis
alcohol
smoking
advanced age
aflatoxin exposure
fam history
alpha-1 antitrypsin deficiency
hereditary tyrosinosis
glycogen storage disease
drugs: oral contraceptive pill, anabolic steroids
porphyria cutanea tarda
male sex
diabetes mellitus, metabolic syndrome
```
89
what are the features of hepatocellular carcinoma?
```
fatigue
fever
weight loss
lethargy
dull ache in the right upper abdomen
OE - irregular enlarged craggy and tender liver
```
90
what investigations would you perform for hepatocellular carcinoma?
```
LFTs
clotting profule
AFP (raised in 70% of cases)
USS
staging CT scan
Biopsy
```
91
what saging can be used for hepatocellular cancer?
Barcelona clinic liver cancer
92
what scores can be used to assess risk in liver cirrhosis?
The well-known and widely used Child-Pugh score uses parameters of serum bilirubin, albumin, INR, degree of ascites, and evidence of encephalopathy to calculate prognosis of patients with liver cirrhosis.
However, recent scores such as the MELD score have been shown to be a better predictor of mortality. The latest MELD score calculator includes parameters of creatinine, bilirubin, INR, sodium, and the use of dialysis (at least twice per week).
A MELD score can also be used to predict the likelihood of a patient tolerating a potential liver transplant.
93
how is hepatocellular cancer managed?
surgical resection
transplant
Non surgical options
- early HCC - image guided ablation, alcohol ablation
- transarterial chemoembolization (TRACE_
94
what cancers most commonly metastise to the liver?
```
bowel
breast
pancreas
stomch
lung
```
95
what is cholangiocarcinoma?
Cholangiocarcinoma refers to cancer of the biliary system. It can occur at any site along the biliary tree, although predominantly arises in the extrahepatic biliary system.
The most common site for bile duct cancers is at the bifurcation of the right and left hepatic ducts (termed Klatskin tumours). They are typically slow-growing tumours that invade locally and metastases to local lymph nodes, before spreading distally to the peritoneal cavity, lung, and liver.
96
risk factors for cholangiocarcinoma?
Primary sclerosing cholangitis (lifetime risk of 10-20%)
Ulcerative colitis
Infective (Liver flukes, HIV, hepatitis virus)
Toxins (Chemicals in rubber and aircraft industry)
Congenital (Caroli’s disease, choledochal cyst)
Alcohol excess
Diabetes mellitus
97
clinical features of cholangiocarcinoma?
generally asymptomatic until late stage
post hepatic jaundice, pruritis, pale stools and dark urine
RUQ pain, early satiety, weight loss, anorexia and malaise
98
what is courvoisier's law?
Courvoisier’s law states that in the presence of jaundice and an enlarged or palpable gallbladder, malignancy of the biliary tree or pancreas should be strongly suspected as the cause is unlikely to be gallstones. This sign may be present only if the obstructing tumour is distal to the cystic duct.
99
investigations for cholangiocarcinoma?
biochemical tests will confirm obstructive jaundice
tumour markers CEA and CA19-9 may be elevated
USS
MRCP plus biopsy
CT for staging
100
what are different types of pancreatic cancer?
```
ductal carcinoma (90%)
exocrine (pancreatic cystic carcinoma)
endocrine (derived from islet cells)
```
101
where does pancreatic cancer usually spread to?
direct invasion of local structures typically involves the spleen, transverse colon, and adrenal glands. Lymphatic metastasis typically involves regional lymph nodes, liver, lungs, and peritoneum. Metastasis is common at the time of diagnosis.
102
risk factors for pancreatic cancer?
smoking
chronic pancreatitis
family history
late onset diabetes mellitus
103
how does pancreatic cancer usually present?
late presentation
obstructive jaundice
weight loss
abdominal pain
104
what investigations do you perform for pancreatic cancer?
```
FBC
LFTs
CA19-9 - tumour marker with a high sensitivity and specificity for pancreatic role
Abdominal USS
CT
fine needle aspiration for biopsy
```
105
how is pancreatic cancer managed?
radical resecition
head of pancreas tumour - pancreaticoduodenectomy
body or tail - distal pancreatectomy
chemotherapy - adjuvant
if metastatic disease use the folfirinox chemo regime
palliative management
- insertion of biliary stent
- palliative chemo
- manage exocrine insufficiency - give creon
106
what are endocrine tumours of the pancreas associated with?
multiple endocrine neoplasia 1 syndrome
107
what are the different types of endocrine tumour in the pancreas?
Gastrinoma - stimulate release of gastric acid
glucagonoma - increased blood glucose concentration
insulinoma - decreases blood glucose concentration
somatostatinoma - inhibit the release of GH, TSH and prolactin from the anterior pituitary and of gastrin
VIPoma - secretion of water and electrolytes into the gut, relaxation of enteric smooth muscle
108
what are GEP-NETs?
Gastroenteropancreatic neuroendocrine tumours (GEP-NETs) refers to neuroendrocrine tumours originating from neuroendocrine cells in the tubular gastrointestinal tract and the pancreas
Neuroendocrine cells are any cells that receives input from neurotransmitters to release hormones into the bloodstream, allowing for an integration between the nervous and endocrine systems.
