lec 14 Flashcards
Factors Influencing Pancreatic Secretion
Stimulating • Cholecystokinin (CCK) • Secretin • Gastrin • Vasoactive intestinal peptide (VIP) • Cephalic phase of eating
Inhibiting • Glucagon-like peptide-1 (GLP- 1) • Pancreatic polypeptide (PP) • Peptide YY (PYY) • Oxyntomodulin (OXM)
Pancreatitis
Inflammation of the pancreas • Characterized by: - Autodigestation - Edema - Fat necrosis (pancreatic) (around the organ) - Hemorrhage of pancreas
• 2 forms: acute and chronic
Acute Pancreatitis (AP)
USA: ~275,000 admissions per year – Relatively uncommon – Incidence rising • ~80% patients admitted have mild, self-limited disease – Discharged within days of admission – Overall mortality: 2%
• Classification – Diagnostic/clinical (based on symptoms, labs, imaging): • Mild, moderate, severe – Further classification: • Acute interstitial – Gland architecture preserved but edematous – Inflammatory cells prominent • Acute hemorrhagic – Marked necrosis, hemorrhage of tissue – Fat necrosis – Vascular inflammation and thrombosis
Signs & Symptoms
Abdominal pain
• Nausea
• Vomiting
• Low-grade-to-moderate fever
Diagnostic Markers
Elevated pancreatic enzymes 3-fold greater than high end of normal range – ↑ amylase – ↑ lipase • Findings of acute pancreatitis on diagnostic imaging – CT – MRI
What if patient with
mild-to-moderate disease
has been NPO for 5-7
days?
Mild Pancreatitis->
Pain limited
Analgesics, IVF-> START PROGRESSIVE (LOW FAT) ORAL DIET, small diet , small meals (6x/d) low fat to rest organs-> normal diet
Severe Acute Pancreatitis Severe Pancreatitis
Abdominal Pain
NPO
(Pancreatic Rest)
What now?
What Route do you Feed in Severe AP?
enteral nutrition is preferred rote - Feed into where? – o Gastric (NG) if not tolerated then NJ o Jejunum (below the ligament of Treitz) - When do you start feeding? o Anticipated NPO>5 days o Early EN is indicated for severe pancreatitis (are they malnourished at admission) - Type of feed? o Standard polymeric (ASPEN Core 2017) o Semi-elemental (small peptide-based) with medium chain Triglycerides OR ELEMENTAL, LOW FAT - Rate? o Continuous preferred over cyclic - Calories : 25-35kcal/kg - Protein: 1.2-1.5g/kg -
Controversies / Changing Paradigms
Traditionally SAP was treated with TPN
– Transitioned to EN (small bowel)
• Now evolving practice from NJ à NG (gastric) feeding
– Studies comparing NJ vs NG: no differences in outcome measures (death,
pain exacerbation, diarrhea, achievement of energy) Chang et al. Crit Care 2013
– Consensus Guidelines (Mirtallo et al. JPEN. 2012; 36: 284-291)
• Grade B (this practice recommended by multiple international societies and based on
intermediate-to-low level evidence)
– ASPEN Adult Nutrition Support Core Curriculum 2017
• Start with gastric feeds; assess tolerance
EV vs PN in SAP
• EN associated with: – ↓ mortality – ↓ septic complications – ↓ surgical procedures – ↓ hospital LOS • Benefits of using the gut – Trophic action on intestinal wall – Prevention/reduction of bacterial translocation
Is PN Ever warranted: if gut is compromised (contraindication), EN is poorly tolerated, not getting enough , want to prevent iatrogenic malnutrition
Chronic Pancreatitis (CP)
Relapsing or continuing inflammation of the pancreas
• Irreversible morphological changes
– Fibrosis, calcification/stones, loss of islet and acinar cells
• Clinical manifestations
– Abdominal pain + exocrine/endocrine insufficiency
– Pain: intermittent or constant, moderate-to-severe
– Pain increased by food (fatty foods) and alcohol intake; result in anorexia
• Exocrine/endocrine insufficiency associated with
– Steatorrhea
– Weight loss
– Malnutrition
Etiopathogenic Risk Factors
Etiopathogenic risk factors:
- Toxic metabolic (alcoholism, smoking, hypertriglyceridemia…)
- Genetic mutations
- Autoimmune pancreatitis
- Obstructive eg. cancer
- Idiopathic (don’t know)
(trypsinogen enters the lumen and gets activated by brush border membrane and activates other- this way the pancreas doesn’t eat it self)
Exocrine & Endocrine Insufficiency
Exocrine insufficiency:
Attributed to loss acinar cell mass or pancreative duct obstruction
- Decrease digestive enzyme levels
- Ductal bicarbonate secretion
Endocrine insufficiency:
- Destruction of pancreatic parenchyma-|> loss of islet cells (responsible for insulin and glucagon production
Nutrition Implications of Exocrine Insufficiency in CP
Fat maldigestion
– Steatorrhea (fecal fat excretion >7 g/d)
• Occurs when pancreatic lipase secretion <10% normal
– Primary cause of weight loss in CP
• CHO and protein maldigestion
– ↓ amylase secretion à impaired CHO digestion
• Abdo distention, gas, loose stools
– ↓ trypsin secretion à impaired protein digestion
• Fat soluble vitamins (A,D,E,K)
– Serum levels decrease (Dutta et al):
• 38-83% of patients with steatorrhea
• 0-23% of patients without steatorrhea
• Vitamin A and E deficiencies most common
• Clinical manifestations of deficiencies
– Vision (Toskes et al.):
• n=28 pt’s with CP: 42% (with steatorrhea) had retinal function abnormalities
• 25% c/o problems with night vision
– Bone density (Moran et al.):
• n=14 pt’s with severe pancreatic insufficiency & steatorrhea
• 10/14 (72%) had osteopenia; 3/14 (21%) had osteoporosis
Nutritional Management of CP
3-pronged approach:
- Pancreatic enzyme replacement therapy (PERT)
- Assessment/correction of nutrition deficiencies
- Maintenance of adequate dietary intake (avoid alcohol)
Non-dietary treatment: pain management
