Nutritional Support Flashcards
1
Q
What is dumping syndrome?
A
Rapid gastric emptying; when food moves from stomach to duodenum too quickly
2
Q
Accessory organs of digestive system
A
liver, gallbladder, pancreas
3
Q
Roles of GIT
A
- Digestion, absorption, excretion
- Secretion of fluids and enzymes
- Gut hormones (e.g. cholecystokinin CCK)
- Immune function
4
Q
Stomach
A
- stores food and secrete gastric digestive juices
- pH 1.5-2.5; highly acidic environment for chemical breakdown of food and extraction of nutrients
- release intrinsic factors for absorption of Vitamin B12
5
Q
Duodenum (small intestine)
A
- digestive juices from pancreas, liver and gallbladder; breaks down food particle in chyme into glucose, TGs and AAs
- absorption of fatty acids
6
Q
Where is bile produced?
A
Liver
7
Q
Where is bile stored?
A
Stored and concentrated in gallbladder
8
Q
Function of bile
A
Contains bile salts which emulsify lipids
9
Q
Function of pancreas
A
Produces enzymes that catabolise starches, disaccharides, proteins and fats
10
Q
Jejunum
A
- bulk of chemical digestion and nutrient absorption
- most of carbohydrates and AAs absorbed
11
Q
Large intestine
A
reabsorb water from undigested food and process of waste material
12
Q
Liver
A
Digestion of fats and detoxifying blood
13
Q
What controls flow of food?
A
Spincter
14
Q
How much fluid does stomach produce?
A
1-2L/day, containing enzymes, gastric acid and electrolytes
15
Q
If patient has vomiting and diarrhoea, what has to be replenished?
A
fluids and electrolytes
16
Q
Where is cholecystokinin produced?
A
Duodenum, in response to food passage
17
Q
Function of cholecystokinin
A
Stimulates pancreatic contraction to release pancreatic enzymes into intestine
Stimulates liver to produce bile
Stimulates gallbladder to contract to release bile
18
Q
If gallbladder is removed, what is the implication on patient’s diet?
A
low fat diet as bile digests fats
19
Q
What happens to CCK without food?
A
CCK is not produced, gallbladder contraction will be impaired and biliary flow also impaired, resulting in cholestasis
20
Q
Cause of malnutrition
A
Decreased intake/absorption
Increased expenditure losses
21
Q
How does advanced abdominal cancer result in malnutrition?
A
Ascites presses on GIT → cause early satiaty (stomach cannot expand as much) → feels full faster → reduced intake
22
Q
How do cancer chemotherapy result in malnutrition?
A
N/V and taste alterations
23
Q
How do burns, trauma, sepsis result in malnutrition?
A
Increased body expenditure of energy consumption through wound healing and helping to fight infections
24
Q
How do dialysis result in malnutrition?
A
Protein losses
25
Malnutrition leads to? -6
1. Increased complications
2. Poor wound healing
3. Compromised immune status
4. Impairment of organ functions
5. Increased mortality
6. Increased use of healthcare resources
26
Nutritional assessment during screening
ABCD
Anthropometric data (height, weight)
Biochemical data (electrolytes, serum albumin)
Clinical (PMH, physical examination)
Diet history
27
Is serum albumin an indicator of nutritional status?
Insufficient protein levels can lead to decreased production of albumin by liver, BUT can also be affected by inflammatory and fluid overload states
28
Screening tools
3-minute nutrition screening
- mainly in outpatient setting
29
3-MinNS scoring
≥3: nutritional risk
3-4: risk of moderate malnutrition
5-9: severe malnutrition
30
Nutritional assessment tool
Seven-Point Subjective Global Assessment (SGA)
31
SGA rating
7-6: well nourished
5-3: mildly to moderately malnourished
2-1: severely malnourished
32
How is energy usually calculated?
kcal
33
Total energy expenditure is dependent on?
Resting/basal metabolic rate, physical activity, stress factor
34
Modes of energy measurement
1. Indirect calorimetry
2. Weight-based
3. Predictive equations
35
What is the gold standard to measure energy required?
Indirect calorimetry
36
How is indirect calorimetry conducted?
Collection of gas
C6H12O6 + 6O2 → ATP + 6CO2 + 6H2O
37
Weight based energy calculation
25-35kcal/kg for general hospitalised patients
38
Predictive equations only estimate ______.
Basal metabolic rate
Need to adjust for activity and stress factor
39
Protein requirement for healthy adult
0.8g/kg/day
40
Protein requirement for CKD not on dialysis patient
0.6-0.8g/kg/day
41
Protein requirement for patients on HD/PD
1.2g/kg/day
42
Protein requirement for patients on CRRT
Up to 2g/kg/day
43
Definition of Enteral Nutrition
Nutrition provided through the GIT via a tube, catheter, or stoma that delivers nutrients distal to the oral cavity
44
Indications for enteral nutrition - 4
1. Swallowing impairment
2. Mechanical ventilation
3. Altered mental status
4. Motility disorders
45
Types of enteral assess devices
Pre-pyloric (NG, PEG)
Post-pyloric (NJ, PEJ)
46
Advantages of NG tubes - 4
1. More physiologic
2. Higher tolerance to bolus
3. Higher tolerance to wide range of enteral feeds
4. May be used for venting
47
Why is NG tube more physiological?
Bypasses less of GIT
48
Why does NG tube have higher tolerance to bolus feeding?
Stomach acts as a reservoir
49
Why NG tube has higher tolerance for feeds with higher osmolarity?
Stomach has higher fluid content than intestines
50
When should NG tube not be used?
Patients with delayed gastric emptying
51
What is the risk caused by more gastric fluid?
More gastric fluid increases risk of vomiting, which increases risk of aspiration pneumonia
52
Advantage of NJ tube
1. Narrower diameter, less discomfort
2. Minimise aspiration risk
53
When can NJ tube be used?
In conditions that result in dysfunctionality in proximal GIT
54
Disadvantage of NJ tube
Higher risk of tube clogging
55
Modes of enteral feed administration
Bolus and Continuous
56
Is bolus or continuous feeding better tolerated?
Continuous
57
Does bolus or continuous feeding have lower risk of aspiration?
Continuous
58
Advantage of bolus administration of enteral feeds?
- No pump required
- Greater freedom for ambulation
59
Types of EN formula
1. Modular
2. Semi elemental
3. Polymeric
4. Immune-modulating/ Disease-specific
60
Modular
- single nutrients
- used as fortifier; not meant to be a meal replacement
61
Long chain TG will first be absorbed into?
Lymphatic system
62
Medium chain TG will first be absorbed into?
Bloodstream
63
Semi elemental
- Partially/completely hydrolysed nutrients
64
Which patient group is semi elemental EN for?
Patients with impaired GI function, impaired tolerance to standard feeds
65
Semi elemental EN is often high in _____?
Osmolarity; can cause diarrhoea
66
Polymeric
Intact MACROnutrients
67
What is required for polymeric EN?
Sufficiently functional GIT
68
Main feature of Glucerna
Low glycemic index
69
Main feature of Presubin Protein Energy
High protein
70
Main feature of Nepro HP
High protein
71
Main feature of Nepro LP
Low protein, K, P
72
Main feature of NutriFriend
Contains omega-2-fatty acids: EPA/DHA
73
Does patient on dialysis require high or low protein intake?
High
74
Which route of administration is drug-nutrient interaction for EN more commonly associated with?
Continuous
75
Administration of incompatible drugs with EN may cause?
1. Precipitation
2. Curdling, clumping of protein
3. Alteration of dosage form
76
When does curdling, clumping of protein occur?
In contact with acid
77
What drug is known to chelate with cations like calcium?
FQ - Ciprofloxacin
78
How to prevent/mitigate drug-nutrient interaction with EN?
1. Stop feeding, flush access device before and after drug administration
2. Therapeutic alternatives available in appropriate dosage form
79
Common complications of EN
1. Occlusion of feeding tube
2. Tube migration
3. Infection secondary to microbial contamination
4. Aspiration
5. N/V
6. D/C
7. ***** Refeeding syndrome
80
Is occlusion of feeding tube more common in NG or NJ tube?
Jejunal due to smaller diameter
81
What kinds of EN formula is more likely to cause occlusion of tube?
Concentrated
High protein
Fibre-rich
82
How to maximise tolerance to EN?
1. Continuous instead of bolus
2. Use pro kinetic agents
3. Post-pyloric feeding if intolerant to gastric feeding
4. Use isotonic formula
5. Semi elemental or elemental feeds for patients with malabsorption issues
83
Which pro kinetic agents can be used to maximise tolerance to EN?
Metoclopramide
Domperidone
IV Erythromycin
84
Indications of parenteral nutrition
For patients who are unable to receive or tolerate adequate nutrition by the enteral route
- Paralytic ileus
- Small bowel obstruction
- High output/ proximal fistula
- Mesenteric ischemia
85
Types of parenteral access devices
1. Peripheral
2. Central
- Non-tunneled central venous catheter
- Tunneled central venous catheter
- Peripherally inserted central catheter (PICC)
- Port-a-Cath
86
Non-tunelled central venous catheter
- Short tube
- Short lived for ≤2w
- Highest risk of infection
87
Limitation of peripheral access for PN
Frequent resite (q72hrs)
Osmolarity (~900)
- If too high, patient will complain of swelling and pain
88
Composition of PN
Nutrition in its simplest, most elemental form
- Complex sugars →
Dextrose
- Protein → AA
- Fats → TG
89
Total parenteral nutrition vs total nutrition admixture
TPN does not contain lipid
90
Administration of incompatible drugs may cause?
1. Precipitation
2. Loss of drug activity
3. Phase separation of lipid emulsions
4. Toxicity
91
Device-related complications for PN
1. Occlusion in IV catheter
2. Mal positioning
3. Catheter-related bloodstream infection
92
What can cause occlusion in IV catheter?
1. Thrombosis/clotting
2. Inappropriate flushing technique
3. PPT due to drug incompatibilities, crystallisation
4. Lipid residues
93
If PN contains lipid, change administration set every _____ hours.
24 hours
94
Metabolic complications of PN
1. Refeeding syndrome
2. Hyper/hypoglycaemia
3. Fluid overload
4. Intestinal failure associated liver disease (IFALD)
5. Metabolic bone disease
95
How is PN associated with IFALD?
1. Prolonged NIL-BY-MOUTH
2. Fatty liver if overfeeding patient
3. Type of TG being fed to patient
96
MOA of prolonged nil-by-mouth
Lack of CCK → impaired bile flow →
cholestasis
97
MOA of TG fed to patient
LCT is pro-inflammatory and precursor of inflammatory markers → giving pure MCT/LCT over prolongedperiods of time may thus cause liver damage
98
How does newer lipid formulation helps with prevention of IFALD
Newer lipid formulations have SMOF – Soybean (LCT), MCT, Olive oil,
Fish oil → Fish oil balances effects of LCT as it is anti-inflammatory
99
What is the hallmark of refeeding syndrome?
Hypophosphataemia
100
Refeeding causes increase in?
Insulin secretion, which leads to increased glucose uptake, increased utilisation of thiamine, increased uptake of K, Mg, PO
101
Signs and symptoms of refeeding syndrome
Hypokalemia
Hypomagnesaemia
Hypophosphataemia
Thiamine deficiency
Salt and water retention (oedema)
102
Management of Refeeding Syndrome
1.Identify high risk patients
2. Check serum electrolytes at baseline
3. Correct deficiency prior to feeding, defer if electrolytes critically low
4. Administer thiamine supplement
5. Initiate feeding slowly (40-50% energy requirements), gradually increase over next few days
6. Continue to monitor electrolytes, adjust replacement if needed
103
Ethical guiding principles in nutritional support
Autonomy
Beneficence
Non-maleficence
Justice
104
Dietary advice
1. Take small frequent meals with snack in between
2. Consume more protein/caloric dense foods
3. Choose soft, low fibre foods
4. Trying out various oral nutritional supplements to see if taste palatable
105
Dose of thiamine supplement
100mg OD for 5 days
106
