PD Flashcards
What is secondary diabetes?
Secondary diabetes is a form of diabetes caused by another primary disease condition e.g. pancreatic disorders, polycystic ovary syndrome etc.
What are the 3 main functions of the pancreas that are essential for digestion?
3 main functions of the pancreas that are essential for digestion:
* Produce digestive enzymes (from acinar cells)
* Production/secretion of insulin & glucagon (from islet cells-tail of pancreas)
* Bicarbonate secretion for neutralisation of gastric acid
Exocrine function of the pancreas
Exocrine function of the pancreas
* Secretion of digestive enzymes (from acinar cells) which flow into the duodenum:
* Fat: Lipases
* Carbohydrate: Amylases
* Protein: Proteases
* Nucleases: any enzyme that cleaves nucleic acids by breaking phosphodiester bonds between nucleotide molecules
Endocrine function of the pancreas
Endocrine function of the pancreas
* Production and secretion of hormones (from Islets of Langerhans)
* Insulin (Alpha cells): released when blood sugar is high
* Glucagon (Beta cells): released when blood sugar is low
* Somatostatin (Delta cells): controls release of other hormones
Which part of the pancreas are acinar cells mainly found? And what do they secrete?
Acinar cells are mostly found in the head of the pancreas and they secrete digestive enzymes.
Which cells do the islets of langherans contain? Which hormones do they secrete?
The Islets of Langerhans contain: Alpha, Beta, Delta Cells.
Alpha cells secrete: insulin
Beta cells secrete: glucagon
Delta cells secrete: somatostatin
Islets of Langerhans (Islet cells) are found in which part of the pancreas?
Islets of langerhans are found in the TAIL of the pancreas
98% of the pancreas is ? and 2% is
98% of the pancreas is EXOCRINE and 2% of the pancreas is ENDOCRINE
Pancreatic anatomy
Pancreatic anatomy
* Situated behind the stomach
* Connected to the gall bladder via the bile duct
* Connected to the duodenum (small intestine)
What is acute pancreatitis?
Acute pancreatitis is SUDDEN inflammation of the pancreas
NICE GUIDELINES for ACUTE Pancreatitis (minimal information)
NICE GUIDELINES for Acute Pancreatitis:
* Ensure not made NBM. Food not to be withheld unless there is a reason such as vomiting
* Enteral nutrition offered to those with: SEVERE/MODERATELY SEVERE acute pancreatitis. Started within 72h with aim to meet nutritional requirements as soon as possible
* Parenteral nutrition those with: SEVERE/MODERATELY SEVERE acute pancreatitis if enteral nutrition failed/contraindicated.
ESPEN GUIDELINES for ACUTE Pancreatitis (2024)
ESPEN GUIDELINES for ACUTE Pancreatitis (2024)
1. Patients with acute pancreatitis should be considered at
moderate to high nutritional risk, because of the catabolic
nature of the disease & the impact of
nutritional status on disease development.
2. MILD to MODERATE AP: should be screened using validated screening methods e.g. Nutritional Risk Screening e 2002 (NRS-2002);
3. SEVERE AP patients: should always be considered at nutritional risk.
4. Obesity:known risk factor for severe AP, also a disease severity-related nutritional risk.
5. MILD AP: Oral feeding shall be offered as soon as clinically tolerated, independent of serum lipase concentrations.
6. MILD AP: Low-fat, soft oral diet shall be used when reinitiating oral feeding.
7. Inability to feed orally: enteral nutrition preferred to parenteral nutrition.
8. Unable to feed orally: Enteral nutrition should be started within: 24-72h of admission.
9. Enteral nutrition: standard polymeric diet shall be used.
10. Enteral nutrition: NG first choice. NJ if digestive intolerance is present.
11. Parental nutrition: patients unable to tolerate EN, targeted nutritional requirements, or if contraindications for EN exist.
What is CHRONIC Pancreatitis?
CHRONIC Pancreatitis is PROGRESSIVE IRREVERSIBLE pancreatic damage including:
* Fibrosis
* Atrophy
* Calcification
* Dilated, irregular or strictured pancreatic duct
ACUTE Pancreatitis Characteristics/Severity/Mortality Rates
ACUTE Pancreatitis Characteristics/Severity/Mortality Rates
* Sudden inflammation of the pancreas
* Can be episodic in nature
* Severity can vary:
1. Short admission with limited medical/nutritional management
2. Prolonged admission with ICU stay, MOF, glycaemic support & nutritional support
3. Length of stay: Mild 1-2days, Severe: 5-6m: sedation & artificial feeding
* Mortality rate varies on SEVERITY & CAUSE
* 1-3% in mild disease (most cases)
* 13-35% in severe disease
What are the causes of ACUTE pancreatitis?
Causes of ACUTE pancreatitis:
* Gallstones (~50% of cases)
* Alcohol (~25% of cases)
* Blunt abdominal trauma
* Hypertriglyceridaemia
* Infections
* Medications
* Endoscopic Retrograde Cholangiopancreatography (less common)
* Autoimmune
* Idiopathic
What is disease in the TAIL of the pancreas likely to lead to?
Disease in the TAIL of the pancreas is likely to lead to ENDOCRINE INSUFFICIENCY (Type 3c diabetes) as the Islets of Langerhans containing alpha and beta cells are located there.
What is disease in the HEAD of the pancreas likely to lead to?
Disease in the HEAD of the pancreas is likely to lead to PANCREATIC EXOCRINE INSUFFICIENCY where there is minimal or insufficient availability of digestive enzymes.
Why is a low-fat soft oral diet suggested by ESPEN (2024) when reinitiating oral feeding in MILD AP?
In MILD AP: a low-fat soft oral diet is suggested by ESPEN (2024) when reinitiating oral feeding because hyperlipidaemia is the 3rd most common cause of AP. Its also as a precaution just in case the pancreas isn’t working properly.
PENG Acute Pancreatitis Nutritional Requirements: ENERGY
PENG Acute Pancreatitis Nutritional Requirements: ENERGY
* <65 BMI:18.5-30: 26 kcal/kg (Dickerson et al., 1991)
* Early stage of SEVERE disease: 15-25 kcal/day (Meier et al., 2006)
* Stable disease/recovery phase: 25-35kcal/day (Meier et al., 2006)
Acute Pancreatitis Nutritional Requirements: PROTEIN
Acute Pancreatitis Nutritional Requirements: PROTEIN
* PENG General: 1.0-1.5g/kg ABW/day
* Meier et al.: 1.0-1.5 g/kg/day
What did Bevan et al., 2017 ‘Incidence & predictors of oral feeding intolerance in AP: A systematic review, meta-analysis & meta-regression’ find about oral feeding intolerance in AP?
Bevan et al., 2017 ‘Incidence & predictors of oral feeding intolerance in AP: A systematic review, meta-analysis & meta-regression’
* Only 16.3% of 1550 patients (~250) experienced oral feeding intolerance
* This was independent of age, sex or cause of AP
* Suggests oral feeding should be considered independent of the above.
What conflicting evidence did Pothoulakis et al., 2021 find about oral feeding intolerance in AP?
Pothoulakis et al., 2021’s prospective cohort study found:
* 13% of 1233 patients with AP experienced oral feeding intolerance
* Independent of time that feeding was initiated (missing data for some patients)
* Oral feeding intolerance more likely in men, younger patients, active alcohol users (not stastically significant)
* Statistically significant findings: high blood urea nitrogen, high haematocrit levels may predict OFI have a longer hospital stay.
* Systemic inflammatory response syndrome of 2 or greater at 48 h and a nonbiliary acute pancreatitis etiology were independent risk factors for oral feeding intolerance.
ESPEN: state that oral feeding should be initiated as soon as clinically tolerated…what does Pothoulakis et al., 2021 say for this?
Pothoulakis et al. 2021 state that OFI depends on unique patient and disease‐related factors. BUN and haematocrit levels may indicate OFI. ESPEN do not state what is meant by clinically tolerated.
What did Sathiaraj et al., 2008 find when comparing oral feeding with a soft diet to clear liquid diet in MILD AP?
(Clinical trial: oral feeding with a soft diet compared with clear liquid diet as initial meal in mild acute pancreatitis)
Sathiaraj et al., 2008 Comparison of Oral Feeding with a L6 soft diet to clear liquid diet in MILD AP:
* 101 patient randomised to clear liquid or L6 soft diet when oral feeding initiated
* L6 Soft diet: Reduced length of stay (statistically significant p=<0.001)
* L6 Soft diet: Higher consumption of fat and kcal on 1st day (statistically significant p=<0.001)
* Stopping the diet because of pain was similar between both groups
BSG ACUTE Pancreatitis Nutritional Recommendations (2019)
BSG ACUTE Pancreatitis Nutrition Recommendations (2019)
* MILD AP: enteral nutrition should be recommenced as soon as abdominal pain has subsided.
* SEVERE AP: patients should be kept nil by mouth until fully resuscitated, usually after 48H
* SEVERE AP: after 48H: normalenteral diet (if tolerated) or enteral tube feeding should be commenced.
* ENTERAL nutrition PREFERRED over PN:Two meta-analyses:enteral nutrition, decreases sepsis, organ failure, the need for surgical intervention and mortality.
* Post-pancreatic feeding is no longer recommended unless there is mechanical gastric outlet obstruction or the patient is unable to tolerate nasogastric tube feeding.
* Parenteral nutrition should be reserved for patients who are unable to reach nutritional goals with nasojejunal feeding. A delay of up to 5 days in the initiation of parenteral nutrition may be appropriate to allow for restarting of oral or enteral feeding.
* Pancreatic enzyme supplementation should be prescribed to patients with symptoms of pancreatic exocrine insufficiency.
Mortality of CHRONIC Pancreatitis
Mortality of CHRONIC Pancreatitis
* At 10 years: survival rate of 70%
* At 20 years: survival rate of 45%
* Mortality ratio of 3.6 in comparison to someone without
Causes of CHRONIC Pancreatitis
Causes of CHRONIC Pancreatitis
* Alcohol (most common) although other factors are likely to be involved
* Recurrent episodes of ACUTE pancreatitis
* Hypertriglyceridaemia
* Autoimmune diseases
* Medications
* Gallstones
* Idiopathic
Medications suggested to cause pancreatitis
Medications suggested to cause pancreatitis
* azathioprine,
* thiazides,
* sulfonamides,
* furosemide,
* estrogens,
* tetracycline
What are people with CHRONIC pancreatitis at high risk of?
People with CHRONIC pancreatitis are at high risk of:
* Malabsorption
* Malnutrition
* Deterioration in their quality of life
What are the general causes of malnutrition in CHRONIC Pancreatitis?
General causes of malnutrition in CHRONIC Pancreatitis:
* Symptoms
* Physical/Psychosocial issues
* Malabsorption
* High nutritional requirements
* Poor glycaemic control
* Reduced intake
What are the symptoms that cause malnutrition in CHRONIC Pancreatitis?
Symptoms that cause malnutrition in CHRONIC Pancreatitis:
* N & V
* Abdo pain/distenstion
* Constipation & diarrhoea
* Reflux
* Delayed gastric emptying
How does malabsorption cause malnutrition in CHRONIC Pancreatitis?
Malabsorption causes malnutrition in CHRONIC Pancreatitis because there is reduced production of digestive enxymes which leads to diminished nutrient absorption.
Why does poor glycaemic control occur in CHRONIC pancreatitis?
Poor glycaemic control occurs in CHRONIC pancreatitis:
* Damage to Beta cells: less/no insulin produced: unable to control blood sugar
What is zymogen converted to in the gut?
In the gut, zymogen is converted to activated digestive enzymes
What do the following enzymes digest?
Amylase
Trypsin
Lipase
- Amylase: digests starch/carbohydrates
- Trypsin: digests proteins
- Lipase: digests lipids/fats/triglycerides
Clinical Manifestation of Chronic Pancreatitis (nutrition specific)
Clinical manifestations of Chronic Pancreatitis (nutrition specific):
* Malnutrition & malabsorption of fat soluble vits: A, D, E &K
* Fat malabsorption: steatorrhoea
* Diabetes
* Maldigestion: undigested food in stool
* Malabsorption: back pain, nausea, GORD, bloating, flatus, wt loss
Which condition is pancreatitis common in?
Pancreatitis is common in patients with Cystic Fibrosis.
Why does mal absorption & maldigestion occur in Chronic Pancreatitis?
Malabsorption & maldigestion occur in chronic pancreatitis because of:
* Destruction of the pancreatic acinar cells leads to loss of pancreatic enzyme syntheisis
* Lipase is vunerable to this which is why malabsorption of fat is prevalent
What is “Systemic Inflammatory Response Syndrome”?
SIRS (systemic inflammatory response syndrome) is:
* an exaggerated defense response from the body to a harmful stressor.
It causes: severe inflammation throughout the body.
Which can lead to: reversible or irreversible organ failure and even death.
Why are nutritional requirements higher in CHRONIC Pancreatitis?
Nutritional requirements are higher in CHRONIC pancreatitis due to chronic inflammation
What are the symptoms of ACUTE Pancreatitis?
Acute Pancreatitis symptoms:
* sudden severe pain in the centre of the abdomen
* nausea/vomiting
* high temperature of 38C or more (fever)
* increased heart rate
* fast shallow breathing
What are the types of ACUTE Pancreatitis?
Types of ACUTE Pancreatitis:
* Mild: no organ failure, no local or systemic complications, usually resolves within a week
* Severe: single or MOF, often long stays with CC admissions, Mortality rate of 25%.
Characteristics of MILD Acute Pancreatitis
Characteristics of MILD Acute Pancreatitis
* No organ failure
* Usually resolves in a week
* No local or systemic complications
Characteristics of SEVERE Acute Pancreatitis
Characteristics of SEVERE Acute Pancreatitis
* Single or MOF
* Long hospital stays with CC admissions
* Mortality rate of ~25%
Name the medications that can cause ACUTE Pancreatitis
Medications that can cause ACUTE PANCREATITIS:
* Steroids
* GLP-1 Receptor Agonists (medication to manage blood sugar)
* Thiazide diuretics (medication for hypertension)
Which infections cause Acute Pancreatitis?
Infections that can cause ACUTE PANCREATITIS:
* Mumps
* Coxsackie B4 Virus
What is fibrosis?
Fibrosis:
* the development of fibrous connective tissue as a reparative response to injury or damage.
* it may refer to the connective tissue deposition that occurs as part of normal healing or to the excess tissue deposition that occurs as a pathological process
What is atrophy?
Atrophy:
* A decrease in size of an organ or tissue; wasting
What is calcification?
Calcification:
* the hardening of tissue or other material by the deposition of or conversion into calcium carbonate or some other insoluble calcium compounds.
Symptoms of Chronic Pancreatitis
Symptoms of Chronic Pancreatitis
* Nausea/vomiting
* Abdominal pain
* Bloating
* Constipation
* Diarrhoea
* Reflux
* Delayed gastric emptying
* Fatigue
What is a potential psychosocial issue in Chronic Pancreatitis?
Potential psychosocial issue in Chronic Pancreatitis:
Alcohol
What is delayed gastric emptying (gastroparesis)?
Delayed gastric emptying (Gastroparesis:
* Food passes through the stomach at a slower rate than it should
* Motility slows or does not occur at all
* Prevents stomach from emptying properly
How does gastroparesis affect nutrition?
Gastroparesis affects nutrition by:
* Symptoms: nausea, vomiting, abdo pain, acid reflux, reduced appetite, fullness
* Wt loss/ nutrient deficiencies
* Changes in blood sugar levels
Is malnutrition common in CHRONIC PANCREATITIS?
Yes malnutrition is common in CHRONIC PANCREATITIS.
Min et al., 2018 found:
* 31.5% of patients with CP had a MUST score of 1 or more. And Vitamin E (~17%) & Vitamin D (62.5%) deficiency was present.
Olesen et al., 2019 found:
* 17% of patients with CP had sarcopaenia. Many of which (74%) had a normal/overweight BMI (>18.5kg/m2).
Which specific malnutrition related concerns are associated with CHRONIC PANCREATITIS?
Sarcopaenia, MUST Score of 1 or more, Vitamin E deficiency & Vitamin D deficiency are associated with CHRONIC PANCREATITIS.
What is GASTRIC OUTLET OBSTRUCTION?
Gastric Outlet Obstruction:
a condition where something blocks the passage between the stomach and small intestine (pylorus). This blockage prevents food from leaving the stomach and continuing the digestion process.
How many Chronic Pancreatitis patients is Type 3c Diabetes found in?
Type 3c diabetes is found in 5%–10% patients with CP, it is a complex subtype of diabetes which leads to glucagon deficiency and brittle diabetes. (BSG, 2019)
What does glutamine do?
Glutamine:
attenuates the pro-inflammatory cytokine release and is considered to be essential for the growth and function of immune cells
Nutritional Assessment CHRONIC PANCREATITIS (ESPEN)
Nutritional Assessment CHRONIC PANCREATITIS (ESPEN)
Anthropometry
* Not just BMI: presence of sarcopenia in CP
* Skinfold measures, Grip strength, sit to stand
* Malnutrition prevalence is high: Current wt, previous wts, wt loss?
* Ht
* Physical ax: signs of muscle wasting/oedema?
Biochemistry
* ? risk of refeeding?
* Mg?: marker of PEI
* Other proposed markers of PEI: haemoglobin, Alb, prealbumin and retinol binding protein (BSG)
* Marker of blood sugar management: HbA1c
* LFTs: Gallstones?
* Vitamin D
* Vitamin E: nutritional status (BSG)
Clinical
* Adm, PMHx, Meds.
* Stool test: FEL-1? (high sensitivity in severe PEI)
* Abdo ultrasound: Gallstones?
* Bile duct obstruction? Gastric outlet obstruction
* Bone mineral density assessment
* Osteoporosis?
* N&V?
* Symptoms of PEI: diarrhoea, offensive smelling stools, steatorrhoea, bloating, abdo pain,
* Opioids? (constipation/reduced gut motility)
Dietary
* Food groups
* Appetite changes
* Allergies, intolerances
* Low GI foods?
* Fat intake?
* Alcohol?
Environment
Functional/Focus
* Smoker?
Where do 95% of pancreatic cancers occur?
95% of pancreatic cancers in the exocrine component of the pancreas. (Acinar cells: digestive enzymes)
Where does the head of the pancreas sit?
The head of the pancreas sits in the duodenum
What is the most common pancreatic cancer?
The most common pancreatic cancer is: pancreatic adenocarcinoma
Where do 60-70% of adenocarcinomas occur?
60-70% of adenocarcinomas occur in the head of the pancreas
What is adenocarcinoma?
Adenocarcinoma is a type of cancer that starts in the glands that line organs.
Pancreatic cancers are often diagnosed ?
Pancreatic cancers are often diagnosed late
What percentage of pancreatic cancers are resectable at diagnosis?
Only 20% of pancreatic cancers are resectable at the time of diagnosis
What percentage of people survive pancreatic cancer for 10 or more years?
5% of people survive pancreatic cancer for 10 or more years
Pancreatic acinar cell carcinoma makes up ~?% of exocrine pancreatic cancers
Pancreatic acinar cell carcinoma makes up ~5% of exocrine pancreatic cancers
There are an average of ~? new cases of pancreatic cancer each year
There are an average of ~10,450 new cases of pancreatic cancer each year
For pancreatic cancer (exocrine) which treatment is utilised by patients the most?
For pancreatic cancer:
* 28% of patients have curative or palliative chemotherapy
* 10% have surgery to remove tumours
* 5% of patients have curative or palliative radiotherapy
What is a Pylorus Preserving Pancreaticoduodenectomy?
Pylorus Preserving Pancreaticoduodenectomy
* Removal of the: head of the pancreas, duodenum (first portion of the small intestine), gallbladder, common bile duct (partial or full)
* Preservation of the: stomach & pylorus (sphincter that controls passage of food from stomach to small intestine)
What is a Whipple Procedure (Pancreaticoduodenectomy)?
Whipple Procedure:
* Removal of the: head of the pancreas, duodenum (first portion of the small intestine), gallbladder, distal portion of the common bile duct, part of the stomach
Pancreas, bile duct or stomach may be connected to the jejunum
What is a Total Pancreatectomy?
Total Pancreatectomy:
* Entire removal of the pancreas, removal of the duodenum, gallbladder, part of the common bile duct, part of the stomach, ? the spleen.
* The stomach is connected to the jejunum, the bile duct is connected to the jejunum.
What is a Distal Pancreactectomy?
Distal Pancreactectomy:
* Removal of the tail of the pancreas & the spleen
What is the SPLEEN responsible for?
The spleen is a part of the lymphatic system.
It is responsible for
* storing & filtering blood
* producing white blood cells
* fluid level maintenance
* production of antibodies to protect against infection
NICE Pancreatic Cancer Nutritional Guidelines
NICE Pancreatic Cancer Nutritional Guidelines:
* Unresectable pancreatic cancer: Offer enteric-coated pancreatin
* Before and after pancreatic cancer resection: Consider enteric-coated pancreatin
* Unresectable pancreatic cancer: Fish oils not to be used as a nutritional intervention to manage weight loss .
* Pancreatoduodenectomy with a functioning gut: offer early enteral nutrition (including oral and tube feeding) rather than parenteral nutrition.
Whatare pancreatic pseudocysts?
Pancreatic Pseudocysts:
* Collection of pancreatic enzymes, blood & tissue adjacent to the pancreas that usually form due to leakage (extravasation) of pancreatic enzymes from the pancreatic duct into surrounding areas.
What impact do Pancreatic Pseudocysts have?
Pancreatic Pseudocysts can impact patients by:
* Delaying gastric emptying by compression of the stomach
* Jaundice via billiary compression (bile duct of gallbladder)
* Reducing appetite due to abdominal pain
Implications of having part of the stomach removed
Implications of having part of the stomach removed
* Constipation? due to reduced peristalsis/motility?
* Undigested food?
* Reduced capacity for food storage? Becoming fuller quicker?
Which nutrients are absorbed in the duodenum?
Nutrients absorbed in the duodenum:
* Iron
*
What is the stomach responsible for?
The stomach is responsible for:
* temporary storage of ingested food
* mixing and digestion of ingested food
* it continues the process of mechanical and chemical digestion
What is Pancreatin?
Pancreatin:
a prescription medication that contains several digestive enzymes.
Gallbladder removal implications
Gallbladder removal implications:
* Reduced digestion of fat? Lack of availability of fat soluble vits? due to reduction of bile availability?
* Less concentrated bile: continuous leakage in small intestine: laxative effect
What is the gallbladder responsible for?
The gallbladder is responsible for:
* stores and concentrates bile produced in the liver. (Bile aids in the digestion of fat and is released from the gallbladder into the upper small intestine in response to food)
What is the common bile duct responsible for?
The common bile duct is responsible for:
carriage of bile from the liver and gallbladder, through the pancreas, and into the small intestine
What is Gastric Outlet Obstruction?
Gastric Outlet Obstruction:
* Obstruction somewhere between the pylorus of the stomach & the duodenum
* It prevents the stomach’s contents from going beyond the duodenum
* Prevents the rest of the digestive system from carrying out responsibilities
How is Gastric Outlet Obstruction diagnosed?
Gastric Outlet Obstruction is diagnosed by ENDOSCOPY or CT
What are the symptoms of Gastric Outlet Obstruction?
GASTRIC OUTLET OBSTRUCTION Symptoms:
* Nausea
* Vomiting
* Abdo pain
* Weight loss
* Malnutrition
* Fullness/ early satiety
What are some of the causes of GASTRIC OUTLET OBSTRUCTION?
Causes of GASTRIC OUTLET OBSTRUCTION:
* Pancreatic cancer infiltration
* Inflammation in pancreatitis
How is Gastric Outlet Obstruction treated?
Treatment of Gastric Outlet Obstruction:
Duodenal stents: they are self expanding metal stents that open the blocked duodenum
Duodenal stent insertion is quick and can be undertaken as day surgery. However they have a ? life span and require ?
Duodenal stent insertion is quick and can be undertaken as day surgery. However they have a short life span and require replacement
Nutritional management of Duodenal Stents (related to Gastric Outlet Obstruction)
Nutritional management of Duodenal Stents (related to Gastric Outlet Obstruction):
* Post stent insertion: begin with liquid diet, progress to soft/moist foods (dietary tolerance is varied)
* Encouragement to chew well: to avoid stent blockage
* Request pro-kinetics: to avoid delayed gastric emptying
* If gastric-emptying normalises: most are able to tolerate normal diet
* Some patients may need liquid/soft diet longer term. Specific foods may need to be altered or avoided.
* Many patients avoid foods that are harder to digest e.g.: nuts, skins, seeds, sweetcorn, grisly meat (? potential issues with fibre)
* Smaller meals more often (Pancreatic cancer Uk)
* Advise patients not to lie down after meals to aid digestion (Pancreatic Cancer UK)
*
* Continued pain may affect dietary intake
What is a biliary obstruction?
Biliary obstruction:
* Bile duct blockage which causes a build up of bile in the body which leads to jaundice
* Usually caused by infiltration of pancreatic cancer
What is biliary obstruction often caused by?
Biliary obstruction is often caused by pancreatic cancer infiltration
What is bile reinfusion?
Bile reinfusion is collection of bile using an external drain (biliary drain), then putting it back into the digestive system bypassing any narrowing or blockage of the bile ducts. This is done orally (patient drinks own bile) or enterally
What might steatorrhoea lead to if left untreated?
If left untreated steatorrrhoea might lead to weight loss due to fat malabsorption (when your body does not fully absorb essential nutrients).
How can biliary obstruction be treated?
A biliary obstruction can be treated with a biliary stent.
What does bile reinfusion allow for?
Bile reinfusion allows for bile to reach the gut, replace electrolytes and aid fat digestion
When is bile reinfusion indicated?
Bile reinfusion is indicated if bile losses are large
Common reasons for nutrition support in Pancreatic Cancer
Common reasons for nutrition support in Pancreatic Cancer:
* Cancer cachexia
* Nausea/vomiting > greater losses
* Taste changes > reduced appetite
* Pancreatic exocrine insufficiency> unable to digest nutrients
* Delayed gastric emptying
Definition and classification of cancer cachexia
Definition and classification of cancer cachexia:
* Precachexia: Wt loss: </= 5%. Anorexia & metabolic change
* Cachexia: Wt loss >5% or BMI <20 & wt loss >2% or sarcopenia & wt loss >2%. Often reduced food intake/systemic inflammation
* Refractory cachexia: Variable degree of cachexia. Cancer disease both procatabolic & not responsive to anticancer treatment, low performance score, <3months expected survival
Solutions to poor nutritional status in pancreatic cancer
Pancreatic Cancer Post-Surgical Nutrition Support
Pancreatic Cancer Post-Surgical Nutrition Support:
* NJ feeding as first line usually accepted
* NG tube usually in situ for drainage of bile
* Common to see patients with a tube in each nostril
Post-operative delayed gastric emptying is high in which procedures?
Post-operative delayed gastric emptying is high in:
* Whipple Procedure
* Total Pancreactectomy
What are Pancreatic Neuroendocrine Tumours?
Pancreatic Neuroendocrine Tumours:
* Form of cancer that affects neuroendocrine cells in pancreas
* Usually slow growing
* May be functional (produce hormones) or non-functional
What are Insulinomas?
How do they affect the body?
- Insulinomas are insulin secreting neuroendocrine tumours found in the pancreas (>99%)
- They can cause hypoglycaemia due to their random/unregulated insulin release that is not related to the insulin secreted by beta cells
Nutritional management of insulinomas
Nutritional management of insulinomas:
1st Line: Low GI Diet:
* Consumption of low GI foods
* Patient is likely to need 3x CHO containing meals
* Patient is likely to need CHO snacks between meals/before bed
* Some patients will need to wake up at 3am to eat a CHO snack to prevent hypoglycaemia overnight
* Some patients find it difficult to eat amount needed to prevent hypoglycaemia
2nd line: Constarch Therapy
* For patients unable to prevent hypoglycaemia with low GI diet.
* Cornstarch= very low GI (can help to prevent hypos)
* Cornstarch can be administered with: milk, water, yoghurt, smoothies
* Initial dose: 0.5g/kg of body wt every 4-6 hours
* Cornstarch therapy dose/frequency titrated based on glycaemic data
* To be taken in addition to Low GI foods
* Side effects: GI due to intestinal fermentation (issues with tolerance
3rd line: Glycosade
* Glycosade= hydrothermally processed high amylopectin cornstarch
* Evidence suggests: can prevent hypoglycaemia for longer than cornstarch when used for glycogen storage disorder
* Initial dose: 0.5g/kg of body wt every 4-6 hours, titrate as needed based on glycaemic data
* Often better tolerated by gut than cornstarch
* Patients may not find palatable and may struggle with this.
4th line: Enteral nutrition (tube)
* Indicated if unable to prevent HYPOS with other interventions (1st-3rd line)
* NG or NJ if n&v present
* Nausea is likely as the patient is suffering from cancer
* ENT feeding may be required: 24hr, overnight, intermittently. Depends on whether patient is able to prevent HYPOs during the day
* Type of feed: LOW VOLUME & HIGH CHO
* Low volume helps with n&v.
* No fat: reduces requirement for PERT
* First choice at CUH: Fortijuice in a flexitainer fed via pump (33.5g CHO/100ml)
* NG/NJ removed/comes out: immediate readmission necessary
5th line: Parenteral nutrition
* Indicated if unable to tolerate ENT feeding/ ENT feeding impossible due to tumour location or size/ there are clinical contraindications for ENT
* 24HR or intermittent feeding may be required
* More freedom to eat with PN
* Set up at home takes several weeks: logistical issues
* Need to consider: micronutrients, lipids, protein
* Safer if d/c home with PN than NG/NJ. Less likely to come out than ENT feeding.
Nutritional Management of Insulinomas: 1st Line: Low GI Diet
Nutritional management of insulinomas:
1st Line: Low GI Diet:
* Consumption of low GI foods
* Patient is likely to need 3x CHO containing meals
* Patient is likely to need CHO snacks between meals/before bed
* Some patients will need to wake up at 3am to eat a CHO snack to prevent hypoglycaemia overnight
* Some patients find it difficult to eat amount needed to prevent hypoglycaemia
Nutritional management of insulinomas: 2nd Line Cornstarch Therapy
Nutritional management of insulinomas:
2nd line: Constarch Therapy
* For patients unable to prevent hypoglycaemia with low GI diet.
* Cornstarch= very low GI (can help to prevent hypos)
* Cornstarch can be administered with: milk, water, yoghurt, smoothies
* Initial dose: 0.5g/kg of body wt every 4-6 hours
* Cornstarch therapy dose/frequency titrated based on glycaemic data
* To be taken in addition to Low GI foods
* Side effects: GI due to intestinal fermentation (issues with tolerance
Nutritional management of insulinomas: 3rd line: Glycosade
Nutritional management of insulinomas:
3rd line: Glycosade
* Glycosade= hydrothermally processed high amylopectin cornstarch
* Evidence suggests: can prevent hypoglycaemia for longer than cornstarch when used for glycogen storage disorder (what about PC?)
* Initial dose: 0.5g/kg of body wt every 4-6 hours, titrate as needed based on glycaemic data
* Often better tolerated by gut than cornstarch
* Patients may not find palatable and may struggle with this.
Nutritional management of Insulinomas:
4th line: Enteral nutrition (tube)
Nutritional management of Insulinomas:
4th line: Enteral nutrition (tube)
* Indicated if unable to prevent HYPOS with other interventions (1st-3rd line)
* NG or NJ if n&v present
* Nausea is likely as the patient is suffering from cancer
* ENT feeding may be required: 24hr, overnight, intermittently. Depends on whether patient is able to prevent HYPOs during the day
* Type of feed: LOW VOLUME & HIGH CHO
* Low volume helps with n&v.
* No fat: reduces requirement for PERT
* First choice at CUH: Fortijuice in a flexitainer fed via pump (33.5g CHO/100ml)
* NG/NJ removed/comes out: immediate readmission necessary
Nutritional Management of Insulinomas: 5th Line: Parenteral nutrition
Nutritional Management of Insulinomas: 5th line: Parenteral nutrition
* Indicated if unable to tolerate ENT feeding/ ENT feeding impossible due to tumour location or size/ there are clinical contraindications for ENT
* 24HR or intermittent feeding may be required
* More freedom to eat with PN
* Set up at home takes several weeks: logistical issues
* Need to consider: micronutrients, lipids, protein
* Safer if d/c home with PN than NG/NJ. Less likely to come out than ENT feeding.
Dextrose could ? insulin secretion if direct in vein via PN
Dextrose could increase insulin secretion if direct in vein via PN
What are Gastrinomas?
Gastrinomas are cancerous tumours that secrete gastrin which facilitates the release of hydrochloric acid from the parietal cells in the stomach. This leads to too much acid being produced in the stomach.
What is Zollinger-Ellison syndrome?
Zollinger-Ellison syndrome:
a rare disease where gastrinomas cause the stomach to produce too much acid, resulting in peptic ulcers. Gastrinomas can grow in the pancreas, small intestine or stomach.
What does Zollinger-Ellison syndrome cause?
Zollinger-Ellison syndrome causes:
* peptic ulcers
* abdominal pain
* diarrhoea
* steatorrhoea (HCl leaves the stomach and denatures enzymes)
Why does steatorrhoea occur in Zollinger-Ellison syndrome?
Steatorrhoea occurs in Zollinger-Ellison syndrome because high amounts of HCl leads to it leaving the stomach and denaturing enzymes so they are unable to do their job.
What is the first line of treatment for Gastrinomas/Zollinger-Ellison syndrome?
The first line of treatment for Gastrinomas/Zollinger-Ellison syndrome are usually PROTON PUMP INHIBITIORS
Use of PPIs may affect the status of which vitamins/minerals?
PPI use may lead to deficiencies in:
iron, vitamin B12, magnesium and calcium
Other than PPIs what type of treatment may patients with gastrinomas/ zollinger-ellison treatment require?
Patients with gastrinomas/zollinger-ellison may also need PERT optimisation if steatorrhoea is present
What is a VIPoma?
VIPoma:
* Vasoactive intestinal polypeptide producing tumours.
* ~90% of them are found in the non-beta islet cells of the pancreas (alpha & delta)
* VIP stimulates the release of water into pancreatic juices, increases secretion of electrolytes, increases motility through the digestive tract & stimulates glycogenolysis in the liver.
What does Vasoactive Intestinal Polypeptide stimulate?
Vasoactive Intestinal Polypeptide stimulates:
VIP stimulates the release of water into pancreatic juices, increases secretion of electrolytes, increases motility through the digestive tract & stimulates glycogenolysis in the liver. This causes watery diarrhoea, hypokalaemia and impaired glucose tolerance.
What symptoms are caused by excessive production of vasoactive intestinal polypeptide?
Vasoactive intestinal polypeptide (VIP) causes:
* watery diarrhoea
* hypokalaemia
* impaired glucose tolerance
This is due to VIP stimulating the release of water into pancreatic juices, increasing secretion of electrolytes, increasing motility of the digestive tract and genolysis in the liver.
Dietetic input for management of VIPoma (Vasoactiver Intestinal Polypeptide) may include?
Dietetic input for management of VIPoma (Vasoactiver Intestinal Polypeptide) may include:
* oral nutrition support: increased losses (watery diarrhoea), liver glycogenolysis, impaired glucose tolerance
* rehydration advice (e.g. dioralyte): watery diarrhoea, hypokalaemia
What are somatostatinomas?
Somatostaniomas:
* Somatostatin producing cancerous tumours of the delta cells in the Islets of Langerhans
* Commonly found in the head of the pancreas
What might patients with somatostatinomas present with?
Patients with somatostatinomas may present with:
* Elevated glucose levels due to insulin inhibition (somatostatin inhibits the release of other hormones)
* Steatorrhoea due to cholecystokinin (CCK) inhibition which is responsible for stimulating digestive enzyme production
Potential dietetic input needed for patient with Somatostatinomas
* Elevated glucose levels
* Steatorrhoea
Potential dietetic input needed for patient with Somatostatinomas
* Elevated glucose levels: first line diabetes advice, CHO consumption
* Steatorrhoea: PERT needed with dietitian input for optimisation
What is a Glucagonoma?
Glucagonoma:
* A glucagon producing cancerous tumour
* Raises blood sugar levels by stimulation of glycogenolysis and gluconeogenesis in the liver
* Causes hyperglycaemia & wt loss (glucose lost in urine)
What do Glucagonomas do?
Glucagonomas:
* Due to secretion of glucagon, glucagonomas raise blood sugar levels via stimulation of glycogenolysis and gluconeogenesis in the liver
* This causes hyperglycaemia and wt loss due to glucose loss in the urine
Which symptoms are associated with Glucagonomas?
Symptoms associated with Glucagonomas:
* Hyperglycaemia
* Wt loss (glucose lost in urine)
Patients with Glucagonomas might need what dietetic input?
Patients with Glucagonomas may require dietetic input that provides:
* Dietary education about CHOs: manage hyperglycaemia
* Dietary education about portion control: manage hyperglycaemia
* ONS: wt loss
Sites & digestive enzymes
Sites & digestive enzymes:
Saliva
* Amylase: CHO
* Salivary lipase: Lipids
Gastric secretion
* Gastric amylase: CHO
* Gastric lipase: lipids
* Pepsin, Rennin, Gelitanase: Protein
Pancreatic secretion
* Amylase: CHO
* Lipase: Lipids
* Trypsin, Chymotrypsin, Carboxypeptidase, Elastase: Protein
Jejujunal/Ileal secretion
* Sucrase, Maltase, Isomaltase, Lactase: CHO
* Intestinal lipase: Lipids
* Brush border proteases: Protein
What is Pancreatic Exocrine Insuffiency?
Pancreatic Exocrine Insufficiency (PEI):
* A reduction or absence of pancreatic enzyme production
How doe enzymes flow in the pancreas?
In the pancreas, enzymes flow from the head to the tail
How do the following pancreatic disorders cause PEI?
* Acute pancreatitis
* Chronic pancreatitis
* Pancreatic cancer
* Surgery
How the following pancreatic disorders cause PEI?
* Acute pancreatitis: short term disruption to enzyme production (episodic)
* Chronic pancreatitis: scarring & damage to enzyme producing (acinar) cells (irreversible)
* Pancreatic cancer: fibrosis of the gland, tumour causing obstruction of pancreatic duct.
* Surgery: removal of bulk of enzyme producing (acinar) cells
What is the most common symptom of Pancreatic Exocrine Insufficiency?
The most common symptom of Pancreatic Exocrine Insufficiency:
Steatorrhoea.
What are some signs and symptoms of Pancreatic Exocrine Insufficiency?
Signs & symptoms of pancreatic exocrine insufficiency (Patient may not have all):
Stool symptoms
* Steatorrhoea
* Pale stools (possibly yellow, orange or white)
* Loose stools (T6 or T7 possibly)
* Frequent bowel movements with urgency
* Very foul smelling stools
- Abdo pain
- Bloating/ abdominal distension
- Reflux
- Burping
- Wind
- Wt loss
- Vitamin (A,D,E,K) & mineral deficiency
Which type of diet might mask PEI?
A low fat diet may mask Pancreatic Exocrine Insuffiency.
How is Pancreatic Exocrine Insufficiency diagnosed?
Pancreatic Exocrine Insufficiency diagnosis:
* Quantitative faecal fat test: gold standard (not common in clinical practice)
* Faecal elastase 1 test (FE-1): indicative of exocrine pancreatic function as it is produced by acinar cells
* Signs & symptoms
Pancreatic Exocrine Insufficiency diagnosis: Quantitiative Faecal Elastase Test
Pancreatic Exocrine Insufficiency: Quantitiative Faecal Elastase Test
* Gold standard
* 72h faecal specimen collection after strict diet of 100g fat/per day for 5 days
* Amount of fat in stools in analysed
* Unpleasant for pt & lab staff
* Rarely used in clinical practice
Pancreatic Exocrine Insufficiency diagnosis: Faecal Elastase 1 Test (FE-1)
Pancreatic Exocrine Insufficiency diagnosis: Faecal Elastase 1 Test (FE-1):
* Measures form of elastase produced by acinar cells in pancreas (stable throughout digestive tract) indicative of exocrine function
* One of stool sample (no specific diet required)
* Commonly used in clinical practice
* Results can be affected by watery stools (dilute true value)
* Not reliable in neuroendocrine tumours or post-pancreatic resection
* Not affected by PERT
* Good at detecting: moderate/severe PEI (not for mild)
Pancreatic Exocrine Insufficiency diagnosis: Signs & Symptoms
Pancreatic Exocrine Insufficiency diagnosis: Signs & Symptoms
* Signs and symptoms: steatorrhoea, T6/T7, foul smelling stool, wt loss etc.
* Can be considered if FE1 is normal and other causes are excluded
* Trial of treatment (PERT) to see if symptoms improve to diagnose
What type of diet is NOT suggested to manage PEI?
A low fat diet is NOT suggested to manage Pancreatic Exocrine Insufficiency because:
* could affect intake/absorption of some vits & minerals
* can reduce intake of kcal in population that is already at risk of malnutrition
* pro & cho still need to be digested/absorbed
If someone isn’t digesting/absorbing fat what other things might they not be able to digest or absorb?
If someone isn’t absorbing or digesting fat it is possible that they cannot do the same with protein or CHOs.
Bloating & wind are usually symptoms of the inability to digest/absorb which macronutrient?
Bloating & wind are usually symptoms of the inability to digest/absorb CHOs.
Questions to be asking to detect PEI
Questions to be asking to detect PEI:
* Colour of stools (pale, yellow, orange, white)
* Consistency of stools
* Signs of oil/grease in stools
* Floating stools? (indication of fat)
* Bloating or wind?
* Trigger foods?
* Meds that could mask symptoms (opioids, anti-diarrhoeals)
* Wt changes
* Blood glucose levels (notes)
* Micronutrient deficiencies (notes, may need to request)
* Medications related to blood glucose
* Previous vs now. Diet: time of day?
Incidence of PEI
* Chronic Pancreatitis
* Acute Pancreatitis
* Resectable pancreatic cancer
* Unresectable pancreatic cancer
Incidence of PEI
** Chronic Pancreatitis**
* Progressive: very likely when CP has been about for a while
* At diagnosis: 8-22%
* 13-26 years: 44-48%
* 14-36 years: 91-100%
** Acute Pancreatitis**
* With severe AP: >60% patients develop PEI
* 25% of all patients develop long term
** Resectable pancreatic cancer**
* ~12% following central pancreatectomy
* ~20% following distal pancreactectomy
* 20-45% pre-op for head of pancreas tumours
* 70-80% following pancreatic-duodenectomy
** Unresectable pancreatic cancer**
* Progressive
* 50-100%
All PERT capsules are ? coated & ? based
All PERT capsules are enteric coated & pork based
There is currently a national shortage of what?
There is currently a national shortage of Pancreatic Enzyme Replacement Therapy
Products & digestive enzyme contents
Products & digestive enzyme contents:
Creon 25000
* Lipase: 25000
* Amylase: 18000
* Protease: 1000
Pancrex V Powder
* Lipase: 25000
* Amylase: 30000
* Protease: 1400
Nutrizym 22
* Lipase: 22000
* Amylase: 19800
* Protease: 1100
Creon 10000
* Lipase: 10000
* Amylase: 8000
* Protease: 600
Pancrex V Capsule
* Lipase: 8000
* Amylase: 9000
* Protease: 460
Creon Micro
* Lipase: 5000
* Amylase: 3600
* Protease: 200
Creon 25000 enzyme contents
Creon 25000
* Lipase: 25000
* Amylase: 18000
* Protease: 1000
What is the common starting dose of PERT?
Common starting dose of PERT:
* Main meals: 44000-50000 lipase units (2x Creon 25000)
* Snacks: 22000-25000 lipase units (1x Creon 25000)
Pert is needed for foods containing ?, ?, ?, including ONS
Pert is needed for foods containing fat, CHO, PRO, including ONS
Which type of foods don’t need PERT to be taken with them?
Foods that don’t need PERT:
* Tea/ Coffee (minimal/no milk)
* Fruit juice, fruit squash, fizzy drinks (fruit smoothies need PERT)
* Sugary sweets (e.g. wine gums, fruit pastilles, jelly babies, mints)
* Alcoholic beers (unless they contain milk, egg, heavy beers such as stout)
* Small amounts of fruit/root veg (bananas may need)
* Fortijuice/Ensure plus Juce (no fat)
Optimal way to take/store PERT
Optimal way to take/store PERT:
* Storage: <25 degrees to prevent enzyme denaturation
* Storage: in container it came in
* Storage: use of cool bags in hot weather
* Storage: not next to body e.g. pocket
* Adm: swallowed whole with a COLD drink (prevent enzyme denaturation)
* Adm: with meals, not before or after. Spaced throughout meal
* Struggling to swallow: can be sprinkled on yoghurt/acidic fruit puree/ketchup
* Dysphagic: Powder form can be taken
* No maximum dose but high PERT can irritate anus?
On wards, self management of ? is recommended
On wards, self management of PERT is recommended
Circumstances where MORE PERT is likely to be needed
Circumstances where MORE PERT is likely to be needed:
* High fat foods: cheesy, creamy, oily, greasy
* Red meat
* Pastries
* Takeaways
* Larger portions
What is advised when more PERT is needed?
There is no guide for when more PERT is needed. It is based on an individuals symptoms. A double dose may be needed for high fat meals. Larger portions may need x2, x3, x4 the dose.
Enteral Feeding with PERT
Enteral Feeding/ NBM with PERT:
* Pancrex V Powder
* 1g Pancrex V mixed with 50ml sterile water.
* If break: pre & post feed
* No break: every 2 hours of feeding
* Peptide based feed usually best: less digestion required
A study comparing early EN, late EN and TPN found what? (Song et al.)
Song et al.
- 10 trials (1051 patients) comparison of early EN (within 48h), late EN & TPN
- Comparing early EN (~48H), late EN & TPN
- In early EN:
- * 47% reduction in mortality (low quality evidence: not statistically significant)
* 42% reduction in MOF (moderate evidence)
* 50% reduction in need for operative intervention (moderate evidence)
* 25% reduction in systemic infection
* 58% reduction in local septic complications
* 16% reduction in GI symptoms (very low quality evidence: patients had mild AP)
* 13% reduction in systemic inflammatory response syndrome
However: 24% increase in other local complications.
