Gastroenterology - Diseases of the pancreas Flashcards Preview

Year 4 - SPM > Gastroenterology - Diseases of the pancreas > Flashcards

Flashcards in Gastroenterology - Diseases of the pancreas Deck (35):
1

What are the different types of pancreatitis?

Pancreatitis is divided into acute and chronic. Acute pancreatitis occurs on the background of a previously normal pancreas and the pancreas returns to functionally and structurally back to normal after the episode. It occurs as isolated or recurrent attacks.

In chronic pancreatitis, there is continuing inflammation with irreversible structural changes. In practice it is not always possible to separate acute from chronic forms because the acute causes (if untreated) may eventually lead to chronic pancreatitis and there may be relapses of the chronic condition - "acute on chronic pancreatitis"

2

What is the prognosis in acute pancreatitis?

Most patients will recover from the attack with only general supportive care, but 25% will develop severe acute pancreatitis with multiorgan failure and about 20% of these patients die.

3

Name some causes of acute pancreatitis

"I GET SMASHED"
Idiopathic
Gallstones
Ethanol
Trauma (e.g. post ERCP, post surgical)

Steroids
Mumps
Autoimmune
Scorpion bites
Hypercalcaemia/ hypertriglyceridaemia (metabolic conditions)
ERCP
Drugs (azothioprine, oestrogens, didanosine)

4

What is the pathogenesis of acute pancreatitis?

Whatever the cause, the final common pathway is marked elevation of intracellular calcium leading to activation of intracellular proteases and the release of pancreatic enzymes. Acinar cell injury and necrosis follows, which promotes migration of inflammatory cells from the microcirculation into the interstitium.

Release of a variety of mediators and cytokines leads to a local inflammatory response and sometimes a systemic inflammatory response that can result in single or multiple organ failure.

5

What are the clinical features of acute pancreatitis?

Usually epigastric or upper abdominal pain radiating through to the back, associated with nausea and vomiting.

On examination:
- epigastric or general abdominal tenderness
- guarding
- rigidity
- be wary of other symptoms (e.g. coma, multiorgan failure) that may dominate the clinical picture
- Ecchymoses around the umbilicus (Cullen's sign) or in the flanks (Grey-Turner's sign) indicate severe necrotizing pancreatitis

6

What blood tests should be performed in pancreatitis?

- Raised serum lipase or amylase in conjunction with an appropriate history and clinical signs, strongly indicates a diagnosis of acute pancreatitis. Normal levels of amylase occur if the patient presents late when urinary amylase or serum lipase levels may still be raised
- FBC, CRP, U&E, LFT, Ca++, and ABG are also measured on admission and at 24 and 48 hours and used to assess the severity of pancreatitis

NB - amylase can also be raised in acute cholecystitis, perforated peptic ulcer and intestinal ischaemia, but very high levels (i.e. >3 times normal) are diagnostic

7

What is the Glasgow criteria?

Glasgow criteria for pancreatitis grades severity and predicts the likelihood of a poor prognosis. Three or more factors present during the first 48 hours predict a severe episode. These include: "PANCREAS"

PaO2 <8.0kPA
Age >55
Neutrophilia >15
Calcium <2
uRea >16
Enzymes - LDH, aminostransferase
Albumin <30 g/L
Sugars (BM >10)

8

What imaging should be requested in cases of suspected pancreatitis?

An erect CXR is performed to exclude perforated peptic ulcer as the cause of the pain and raised amylase.

Abdominal US is performed as a screening test to look for gallstones as a cause of pancreatitis and may show swelling of the inflamed pancreas.

Contrast enhanced spiral CT scanning or MRI is performed in all but the mildest attack of pancreatitis to confirm the diagnosis, identify the presence and extent of pancreatic necrosis (associated with organ failure and higher mortality) and identify peripancreatic fluid collections. It is performed after 72 days as early CT may underestimate the severity of pancreatitis.

9

How should patients with pancreatitis be managed?

Risk stratification is essential as management depends on severity. Glasgow criteria, Ranson's criteria and the acute physiology and chronic health evaluation score (APACHE) are acceptable tools. Obesity and a CRP >200 mg/L in the first 4 days are also associated with a worse outcome.

If predicted severe disease:
- medical therapy
- HDU or ITU
- prophylactic antibiotics
- nasogastric feeding
- ERCP within 48 hours if gallstone pancreatitis and/or cholangitis
- contrast enhanced CT/ MRI within 3-7 days
- monitor for complications

If predicted mild disease:
- medical therapy (pain control, NBM, IV fluid, NG tube)
- monitor for complications

10

What general supportive care should be offered to patients with acute pancreatitis?

Early fluid replacement is essential and in severe pancreatitis 5L or more of crystalloid daily may be required to maintain adequate urine output (>0.5ml/kg body weight/ hour).

Supplemental oxygen is given and requirements are guided by pulse oximetry and ABGs.

LMWH is given to prevent DVT.

Electrolyte and metabolic abnormalities are corrected and a sliding scale (variable rate) insulin infusion may be necessary for control of blood glucose.

Pain is controlled by pethidine and tramadol and a patient controlled system is necessary if persistent. Morphine is avoided because it increases sphincter of Oddi pressure and may aggravate pancreatitis.

In patients with predicted severe attacks, there is a likelihood of oral nutrition for a number of weeks. Nutrition is provided by a nasogastric tube or nasojejunal tube (placed endoscopically) for patients who are intolerant of nasogastric feeding due to exaccerbation of pain or nausea and vomiting.

11

What therapies can be given in acute pancreatitis to reduce the severity or frequency of complications?

Broad spectrum antibiotics - e.g. cefuroxime or aztreonam, reduce the risk of infection of the necrotic pancreas and are given from the outset. Early ERCP (within 48-72 hours) and sphincterotomy improves the outcome in patients with biliary pancreatitis and evidence of cholangitis or a high suspicion of CBDstone (dilated CBD or CBD stone seen on US or jaundice) or when pancreatitis is predicted to be severe.

Surgical treatment is sometimes required for very severe necrotising pancreatitis, particularly if it is infected or if complications such as pancreatic abscesses or pseudocysts appear.

12

What are the complications of acute pancreatitis?

Hyperglycaemia
Hypocalcaemia
Renal failure
Shock

13

What causes hypovolaemic shock in pancreatitis?

Third space extravasation. Third space fluid is sequestered fluid that is unavailable for maintaining volume in the vascular compartment. In acute pancreatitis, it refers to the peripancreatic collection of fluid that commonly occurs as the pancreas autodigests itself. If conditions improve, the third space fluid gains entry back into the vascular compartment and may cause fluid overload.

14

What causes hypoxaemia in pancreatitis?

Circulating pancreatic phospholipase destroys surfactant.
Loss of surfactant induces atelectasis and intrapulmonary shunting, which produces a V/Q mismatch.

ARDS may also occur.

15

What is a pancreatic pseudocyst?

This is a complication of pancreatitis in 20% of cases. It is a collection of digested pancreatic tissue around the pancreas. It presents as an abdominal mass with a persistence of serum amylase >10 days (amount of amylase in the fluid surpasses the renal clearance).

Treatment depends on the size, if <5cm, observe and follow with CT scan. Most resolve without surgical intervention. If >5cm, treat with CT or US guided drainage.

16

What findings are associated with a pancreatic abscess?

Again this is a complication of acute pancreatitis. Clinical and laboratory findings include abdominal pain, high fever due to sepsis (usually gram negative infections such as E.coli), neutrophilic leukocytosis and persistent hyperamylasaemia.

Diagnosis is by CT, which shows multiple radiolucent bubbles in the retroperitoneum. CT guided aspiration of abscess identifies the organism. Treatment is with Imipenem and surgical drainage.

17

What features suggest pancreatic necrosis?

Systemic signs earlier than usual
Higher fever than usual; sinus tachycardia
Greater degree of neutrophilia
Peripancreatic infections occur in 40-70%.

18

What is the pathogenesis of chronic pancreatitis?

Inappropriate activation of enzymes within the pancreas leads to precipitation of protein plugs within the duct lumen, forming a nidus of calcification. Subsequent duct blockage leads to ductal hypertension and further pancreatic damage. This together with cytokine activation leads to pancreatic inflammation, irreversible morphological change and/or permanent impairment of function. The commonest cause of chronic pancreatitis in most developed countries is alcohol. Other causes are tropical pancreatitis, and hereditary, autoimmune and cystic fibrosis.

19

What are the clinical features of chronic pancreatitis?

Epigastric abdominal pain, either intermittent or constant, and radiating through to the back is the commonest symptom. There may be severe weight loss as a result of anorexia. Diabetes and steatorrhoea develop due to endocrine (insulin) and exocrine (lipase) insufficiency.

Occasionally jaundice is the presenting complaint due to obstruction of the CBD during its course through the fibrosed head of pancreas. The differential diagnosis is from pancreatic carcinoma, which also presents with pain and weight loss and may develop on the background of chronic pancreatitis. Carcinoma should be considered when there is a short history and localised ductular abnormalities on imaging.

20

How is chronic pancreatitis diagnosed?

Diagnosis is made by imaging (to demonstrate structural changes in the gland) and metabolic studies which demonstrate functional abnormalities.

21

What imaging is required in chronic pancreatitis?

A plain abdominal X ray will show pancreatic calcification in some cases. US and CT scanning may show calcifications, ductal dilatation, irregular inconsistency and outline of the gland and fluid collections. CT is more sensitive test than US. MRCP and endoscopic US are sometimes used if the diagnosis is not confirmed with other imaging tests. ERCP is usually reserved for therapeutic - e.g. pancreatic stent placement, rather than diagnostic purposes.

22

What functional assessments should be undertaken to diagnose chronic pancreatitis?

These tests are insensitive in early pancreatic insufficiency:
- faecal elastase - measured on a single random stool sample, is reduced
- other tests rely on measuring decreased concentrations of the products of synthetic compounds
- serum amylase is not of use in diagnosing chronic pancreatitis, but may be raised during an acute episode of pain
- raised BM

23

How is chronic pancreatitis treated?

- Advise on alcohol cessation
- Pain require opiates to control
- Surgical resection combined with drainage of the pancreatic duct into the small bowel (pancreaticojejunostomy) is of value in severe disease with intractable pain
- Pancreatic strictures or stones are sometimes amenable to endoscopic treatment with ERCP
- Persistent pseudocysts are drained endoscopically into the stomach or by surgical drainage
- Pancreatic enzyme supplements are useful for those with steatorrhoea and may reduce the frequency of attacks of pain in those with recurrent symptoms
- Diabetes requires treatment with diet, oral hypoglycaemics or insulin

24

What is the epidemiology of pancreatic carcinoma?

Men are affected more commonly than women
Incidence increases with age, most cases occur in the over 60s
Most are ductal adenocarcinomas

25

What is the aetiology of pancreatic carcinoma?

Hereditary (a dominant susceptibility gene in some families and other susceptibility genes in defined syndrome) and environmental factors (smoking and obesity) both contribute. Chronic pancreatitis is also premalignant, particularly in patients with hereditary pancreatitis.

26

What are the clinical features of pancreatitis?

Cancer affecting the head of pancreas or ampulla of Vater presents with painless jaundice as a result of obstruction of the CBD and weight loss. On examination there is jaundice with characteristic scratch marks and a distended, palpable gall bladder (Courvoisier's law: if in cases of painless jaundice the gall bladder is palpable, the cause will not be gallstones). In gallstone disease, chronic inflammation and fibrosis prevent distension of the gall bladder. There may be a central abdominal mass..

Cancer of the body or tail presents with abdominal pain, weight loss and anorexia.

Diabetes may occur and there is an increased risk of thrombophlebitis. Patients can also present with non specific signs - e.g. an elderly patient with a change in bowel habit and dyspepsia.

27

How is pancreatic cancer diagnosed?

Diagnosis is made by US (which demonstrates dilated bile ducts and a mass lesion) and/or contrast enhanced spiral CT; the latter is more sensitive test particularly for body and tail tumours and is almost always necessary to stage cancer. MRI and endoscopic US is used for staging (endoscopic US) and in difficult cases for diagnosis.

ERCP is usually restricted to palliative treatment (e.g. bile duct stenting in a jaundiced patient) but may provide a source of cytology to make the diagnosis. The tumour marker CA19-9 is sensitive but not specific for diagnosis. Serial measurements are usually made to check response to treatment.

28

How is pancreatic cancer treated?

Surgical resection offers the only hope of cure but few patients have resectable disease at diagnosis. Tumour adherence or invasion into adjacent structures, particularly major blood vessels (locally advanced disease), makes complete resection dif cult, and these patients are treated with combined chemotherapy and radiotherapy. 5-Fluorouracil and gemcitabine improve survival in advanced disease and also increase survival as an adjuvant therapy to pancreatic resection. Palliative treatment is often necessary for patients with unresectable pancreatic cancer to relieve obstructive jaundice (usually by endoscopic placement of a stent across the obstructed distal CBD), gastric outflow obstruction, and pain.

29

What is the prognosis of pancreatic cancer?

Overall, the prognosis is very poor. For the few patients who have had surgical resection with curative intent the 3-year survival is 30–40%. The median survival for treated patients with locally advanced disease is 8–12 months and for patients with metastatic disease it is 3–6 months.

30

What is the name given to cancer of the bile duct?

Like pancreatic cancer, cholangiocarcinoma is also a disease of the elderly with a poor prognosis. It occurs more frequently in patients with primary sclerosing cholangitis, congenital bile duct abnormality and infections with liver fukes e.g. Clonarchis sinensis. Presentation is usually with jaundice secondary to bile duct obstruction or with metastatic disease. Imaging by US, CT or MRI shows a bile duct stricture, a hilar mass or multiple metastases.

31

What are neuroendocrine tumours of the pancreas? How are they diagnosed?

Islet cell tumours are rare and usually produce their clinical effect by hormone production. Non-functioning tumours present with pain and weight loss. Circulating hormone concentrations, e.g. gastrin, can be measured in the serum and high levels help to make the diagnosis. Most neuro- endocrine tumours express large numbers of somatostatin receptors and radiolabelled somatostatin analogue scanning (111In-labelled octreotide) pro- vides a means of tumour localization.

32

How are neuroendocrine tumours treated?

Treatment is by excision of the primary tumour if possible. Symptomatic treatment (e.g. high-dose proton pump inhibitors for gastrin- omas) and chemotherapy or hepatic artery embolization are used for patients with hepatic metastases.

33

How does Zollinger-Ellison syndrome present?

Duodenal ulceration - recurrent and severe
Diarrhoea - hypersecretion of gastric acid inhibits digestive enzymes

34

What is a VIPoma?

This is a tumour secreting vasoactive intestinal peptide (VIP). It typically presents with severe watery diarrhoea and hypokalaemia due to stimulation of intestinal water and electrolyte secretion.

35

How does a glucagonoma present?

Migratory necrolytic dermatitis, weight loss, diabetes mellitus, deep venous thrombosis

Decks in Year 4 - SPM Class (129):