Fundamentals of Nutrition & Metabolism Flashcards
What is the length range for the small bowel in adults?
400 to 800 cm
(T/F) <100 cm without colon requires TPN
TRUE
(T/F) <50 cm with colon requires TPN
TRUE
(T/F) The small bowel correlates with weight.
FALSE It correlates with height, shorter length seen in women.
Where does absorption primarily occur for each vitamin:
- Vitamin K
- Vitamin B1
- Vitamin A
- Vitamin B12
- Vitamin K: Jejunum
- Vitamin B1 (thiamine): Proximal small intestine, especially jejunum
- Vitamin A: Upper SI
- Vitamin B12: Mostly ileum
Accumulation of which trace element is associated with Wilson’s disease?
Copper
- Wilson’s disease is characterized by a genetic mutation of copper metabolism.
- Normal copper homeostasis is maintained via biliary excretion.
- Toxicity can occur with impaired biliary excretion
(TRUE/FALSE) The acute phase response to injury and infection suppresses iron transport.
Part 2: What happens to serum iron levels? Serum ferritin levels?
TRUE.
- Serum iron levels decrease
- Serum ferritin levels increase
- The sequestering of iron into a storage form following injury and infection is thought to have several protective measures for the host. It reduces the availability of iron for iron-dependent microorganism proliferation and may reduce the potential for free radical production and oxidative damage to cell membranes and DNA.
Explain enterohepatic circulation.
Refers to the circulation of bile acids, bilirubin from the liver to the bile, followed by entry into the SI, absorption by the enterocyte (in the intestine) and transport back to the liver.
What is Cholecystokinin? What is its function in relation to enterohepatic circulation?
- It is an enteric hormone in the liver.
- Which induces the gallbladder to contract and release bile into the SI, when fat and protein is present in the duodenum
The majority of dietary folate is reabsorbed via which mechanism?
What conditions may limit folate absorption?
Enterohepatic circulation.
- Dietary folate is converted to monoglutamate by jejunal enzymes for entry into the intestinal cell. It undergoes further reduction before entry into the portal circulation for reabsorption via enterohepatic circulation.
Conditions that may limit folate absorption?
- Zinc deficiency
- Chronic alcohol consumption
- Changes in jejunal pH
- Impaired bile secretion
Explain the function of choline.
Required for lipid transport and metabolism.
- Used as a treatment for hepatic steatosis.
- Low plasma choline levels in long-term PN patients have been associated with elevated liver aminotransferase concentrations. Investigations reported that steatosis resolved following choline supplementation.
- Currently, PN admixtures do not contain choline.
Name 3 examples of monosaccharides:
Options: Galactose, sucrose, glucose, maltose, fructose, lactose
- Glucose
- Fructose
- Galactose
What is phosphofructokinase?
Rate-limiting enzyme of glycolysis, which is inhibited when ATP is abundant.
Why is the inhibition of phosphofructokinase important when ATP is abundant during glycolysis?
Allows the cell to divert glucose to be stored as glycogen
When ATP is limited, phosphofructokinase is activated.
Glycolysis = Breakdown of glucose
Which two places is glycogen predominantly stored?
Liver
Skeletal Muscle
What measurement is reflective of the functional or long-term status of SELENIUM?
Plasma glutathione peroxidase.
- Deficiency: <10.5 U/mL erythrocytes
- Status can also be assessed by determining the selenium level in whole blood, plasma, serum, or erythrocytes.
- Plasma levels of greater than 100mcg/L = Adequate levels
What measurement does serum ceruloplasmin measure?
Copper status
Explain the function of CHROMIUM.
Chromium potentiates the action of insulin and is important in glucose, protein, and lipid metabolism.
Chromium deficiency impairs glucose and AA use which may result in HYPERGLYCEMIA.
What is a common clinical sign/symptom of vitamin D toxicity?
Soft tissue calcification (may occur in lungs and cardiovasculature).
Other signs: confusion, psychosis, tremor, hypercalcemia, and hypercalciuria
What are common clinical signs/symptoms of vitamin D deficiency?
- Hypocalcemia
- Osteomalacia
- Tetany
- Osteoporosis
What are some effective treatments in gastric phytobezoars?
- Flushing with Cola
- Enzymatic therapy with cellulase
- Surgical removal
Specifically, treatment with PAPAIN (meat tenderizer) should be avoided because it breaks down normal tissue and is associated with peptic ulcer disease, esophagitis, and gastritis.
(TRUE/FALSE)
Fiber and medications can be flushed together through the feeding tube.
FALSE.
Should be spaced apart.
Never manipulate the feeding bag system due to risk of microbial growth through touch contamination
Explain the Swinamer Equation.
Uses body surface area in addition to physiological variables to predict RMR (resting metabolic rate).
This equation has been found to predict RMR in about 55% of patients.
Name some impacts that underfeeding has on critically ill patients.
Increases:
- Infections
- Complications
- Days on antibiotics
- Days on the ventilator
Name some impacts overfeeding has on critically ill patients.
Negative effects:
- Hyperglycemia
- Liver dysfunction
- Fluid overload
- Respiratory compromise
- Increased CO2 production
- Lipogenesis
(FILL IN THE BLANK)
[Insoluble/Soluble] fiber has stool softening effect resulting in faster transit time and more frequent bowel movements which provides relief from constipation.
[Insoluble/Soluble] fiber is fermented in the distal intestines and increases intestinal mucosal growth and promotes water and sodium absorption.
- Insoluble fiber
- Soluble fiber
What is the approximate half-life of albumin?
20 days
What is the approximate half-life of serum prealbumin?
2-3 days
Define metabolic acidosis.
Metabolic acidosis:
pH < 7.35, decreased HCO3-, hyperventilation = dec pCO2
Causes:
H Hyperalimentation/TPN/EN
A Acetazolamide
R Renal Tubular Acidosis (bicarb rich renal loss)
D Diarrhea (bicarb rich fluid loss)
U Ureterostomies
P Pancreatic fistulas (GI loss)
M Methanol
U Uremia
D DKA/Alcoholic KA/Starvation KA
P Paracetamol, acetaminophen, phenformin/paraldehyde
I Iron, Isoniazid, Inborn errors
L Lactic acidosis
E Ethanol, Ethylene glycol
S Salicylates, ASA, aspirin
hyperparathyroidism, hypoaldsteronism)
* Ingestion of ammonium chloride or PN containing chloride salts
Explain the chemical structure of fatty acids.
Molecules with an acidic carboxyl group at one end followed by a long chain of hydrogenated hydrophobic carbon atoms. Each FA is chemically characterized by the number of carbon atoms and double bonds present.
How long are:
- Short-chain FAs
- Medium-chain FAs
- Long-chain FAs
- Very long-chain FAs
- SCFAs (2-4 carbons)
- MCFAs (6-12 carbons)
- LCFAs (14-18 carbons)
- Very long-chain (20 carbons or more)
What type of FA is butyric acid?
SCFA (has 4 carbons)
What type of FA is lauric acid?
MCFA (has 12 carbons)
What type of FA is stearic acid?
LCFA (has 18 carbons)
Explain the basic structure of a triglyceride.
Glycerol backbone with 3 FA molecules attached via an ester linkage.
Triglycerides that require bile acids to facilitate enzymatic digestion and absorption contain FAs that are typically how long?
14 carbons in length.
The overwhelming majority of enteral dietary lipids (~90%) are ingested in the form of triglycerides. FAs of up to 10 carbons in length and glycerol can be absorbed DIRECTLY via the villi of the intestinal mucosa.
Long-chain triglycerides require bile salts for both enzymatic digestion and the formation of micelles.
Where does the oxidation of FAs for ATP production occurs…?
Cells that contain mitochondria.
- Mitochondria are organelles found in most eukaryotes whose primary function is to generate APT via oxidative phosphorylation, the major source of cellular energy.
- FAs are transported into the mito. membrane and through the beta-oxidation pathway the FA is degraded and released as ATP.
(TRUE/FALSE)
Red blood cells DO contain mitochondria in their cytoplasm.
FALSE
RBCs rely on the metabolic pathway of glycolysis for ATP for energy.
What do both linoleic acid and alpha-linolenic acid require to enter the mitochondria?
L-carnitine
Explain the breakdown of water in the body.
- Intracellular
- Extracellular
- Transcellular
TBW (total body water is 50-60% of body weight; broken down into 3 compartments on front).
- ICF = 2/3
- ECF = 1/3
- Intravascular space = 1/4
- Interstitial space = 3/4
What is the best treatment for mild hypercalcemia? Severe hypercalcemia?
- Mild: Usually responds to hydration and ambulation; requiring no further intervention.
- Severe: Initially treated with saline hydration to correct volume depletion; then furosemide after hydration to enhance renal calcium excretion. HD may be necessaary
Absorption of large polypeptides, oligopeptides, and free AAs takes place in the?
Small intestine.
-HCL secreted by the parietal cells of the stomach denatures the protein and makes it more susceptible to enzymatic action. Converts the inactive pepsinogen to active pepsin. Pepsin activates other pepsinogen molecules or hydrolyzes specific peptide bonds into end products of large polypeptides, oligopeptides, and free AAs. This mixture known as acid chyme passes into the duodenum where the majority of protein digestion takes place.
When determining nitrogen balance, urea accounts for what percentage of total urine nitrogen losses?
80%.
-Urinary urea nitrogen concentration is affected by stress and increased urinary excretion of non-urea nitrogen.
Supplemental arginine is considered therapeutic for what?
Immune function and wound healing.
-Supplementation with arginine in the critically ill septic patient population remains controversial.
Transformation of free LCFAs into acylcarnitines and transport into the mitochondria, requires what?
Carnitine.
- It is a trimethyl AA similar in structure to choline
- Primary deficiency is rare, it has been documented in preterm infants and chronic renal failure.
Which organ is key for protein metabolism? Why?
Liver because of its high capacity for uptake and metabolism of aaS.
- About 57% of the AAs extracted by the liver are either oxidized or used to synthesize plasma proteins.
How does soluble fiber control diarrhea?
Soluble fiber has the ability to increase sodium and water absorption via its fermentation byproducts (SCFAs).
What are two symptoms of abdominal discomfort?
Bloating and flatulence
How does insoluble dietary fiber regulate normal defecation?
Increasing stool weight and bulk.
Consumption of soluble fiber contributes to lower what?
Total cholesterol and LDL cholesterol.
- Does not change or lower HDL cholesterol levels
- May result in a small decrease in plasma glucose and A1C.
(TRUE/FALSE)
Soluble fiber lowers the risk of developing colon cancer and reducing the recurrence of adenomas.
FALSE
Currently no clear evidence.
During long-term starvation, what is the main energy source?
Fat acid oxidation.
- Fat tissue becomes the main energy source for nearly all tissues.
- After 14 days of fasting, adipose tissue can provide more than 90% of daily energy requirements.
- Remember: high glucagon concentrations promote FA oxidation
Sodium-glucose transporter 1 (SGLT-1) transports which two substrates into the enterocytes from the intestinal lumen?
Does this require energy?
- Glucose
- Galactose
Yes, energy is provided by hydrolysis of ATP; therefore, is an active transport system.
Which 2 water-soluble vitamins do not require Na+ co-transporters for absorption?
- Vitamin B12
- Requires intrinsic factor (secreted by parietal cells in the stomach) for absorption, taken up by receptors in the distal ileum
- Folic Acid
- Absorbed by a carrier-mediated process, primarily in the proximal part of the small intestine.
How are MCTs absorbed?
They are water-soluble, hydrolyzed and pass through the enterocytes directly into the portal circulation
(TRUE/FALSE)
MCTs require the formation of micelles or bile salts for absorption.
FALSE.
They are water soluble
Mucosal atrophy that accompanies bowel rest may result from an absence of what substrate?
Glutamine, the principal metabolic fuel for intestinal cells
- Atrophic changes during bowel rest have been decreased with glutamine-enriched parenteral nutrition.
What are symptoms of diarrhea, bloating, and flatulence after ingestion of sugar caused by?
Deficiency of brush border oligosaccharidases
- This deficiency allows osmotically active undigested oligosaccharides to cause a shift of water into the intestinal lumen
- Resulting in increased pressure increases further when colonic bacteria act on remaining oligosaccharides, thus increasing the number of osmotically active particles.
- Formation of CO2 and H2 from disaccharides further increase symptoms.
Where does the majority of fat digestion occur?
Duodenum (with pancreatic lipase)
- Begins in the mouth (lingual lipase, ~10%) and stomach (gastric lipase, small amount)
What is the role of bile acids in fat digestion?
Act as emulsifiers
What is pancreatic exocrine deficiency?
The pancreas does not provide the digestive enzymes or they do not work normally
- Symptoms: diarrhea, abdominal pain/distention/bloating/cramps/flatulence/weight loss
- Treatment: Pancreatic enzyme replacement therapy
What AA is conditionally essential and also a primary fuel source for enterocytes?
Glutamine
- Most abundant AA in the body, and vital fuel for rapidly dividing cells
- In some conditions: trauma, sepsis and exercise, the body’s glutamine requirement exceeds the rate of synthesis
- Decreased levels are associated with intestinal mucosal atrophy, impaired immune function, and decreased protein synthesis
What is the average nitrogen content of protein? Calculation?
Has been determined to be 16%
- To calculate nitrogen content of a protein in a PN solution:
- Total grams of protein x 0.16 OR
- Total grams of protein / 6.25
What is the protein recommendation for critically ill patients with trauma? What are two exceptions? What is their recommendation?
1.5 to 2.0 g/kg/day
Exceptions:
- CRRT & BMI > 30 should get 2.0 to 2.5 g/kg/day
- For BMI 30+: use IBW
What are two areas of the body that require a constant supply of glucose?
Brain and RBCs
When does glycogenolysis start during fasting? When are stores depleted?
When is gluconeogenesis started? When does the body switch substrates after this?
Why does the body switch away from gluconeogenesis?
Glycogenolysis (breakdown of hepatic glycogen stores) begins 2-3 hours of fasting; with stores depleted after 24 hours.
Gluconeogenesis (from AA substrate) begins within 4-6 hours after the last meal. After 2 days of starvation, the brain switches its fuel source from glucose to ketone bodies.
The liver converts free FAs to ketone bodies. The adaptation of starvation with a ketone-based fuel system minimizes gluconeogenesis and further protein breakdown.
What are the 3 organs in the body that have the necessary enzymes for gluconeogenesis?
- Liver (main site)
- Small intestine (under certain conditions)
- Kidney (under certain conditions)
Explain AMDR. What 3 nutrients have established AMDRs?
AMDR = Acceptable Macronutrient Distribution Range
- A range of intake for a particular energy source that is associated with reduced risk, rather than assisting in the treatment, of chronic disease.
- Omega-3
- Omega-6
- Total Fat
Explain Tolerable Upper Intake Level.
The highest level of daily nutrient intake that is likely to pose no risk of adverse health effects to almost all individuals in the general population.
Explain EAR.
EAR = Estimated Average Requirement.
- The average daily nutrient intake level estimated to meet half the needs of healthy individuals in a particular life stage and gender group.
What oils are included in commercial enteral formulas to provide a good source of linoleic and alpha-linolenic acids?
- Corn
- Soybean
- Safflower
- Canola oils
What is the prominent clinical change seen with EFAD? What are other implications?
Dry, scaly rash
- Increased susceptibility to infection
- Impaired wound healing
- Weight loss
- Immune dysfunction
(TRUE/FALSE)
The active transport of sodium out of the cell provides the energy for glucose transport.
TRUE
The transport of sodium out of the cell maintains the concentration gradient needed for sodium to shuttle more glucose into the mucosal cells.
Explain pellagra.
Niacin deficiency disease; presents as the 3 ‘Ds’
- Dermatitis
- Diarrhea
- Dementia
Food Sources include: meat, fish, poultry, enriched and fortified breads, and cereals
What is ursodiol?
Ursodiol (ursodeoxycholic acid) is a form of bile acid that may potentially improve fat absorption.
Therefore, it facilitates absorption of fat.
What does sulfamethoxazole/trimethoprim induce?
Hyperkalemia by impairing renal potassium excretion.
What is the first-line therapy for hyperkalemic emergencies?
Calcium gluconate 1-2 grams IV over 10 minutes, with an effective onset time of 1-2 minutes.
Should be given to symptomatic patients or those with ECG changes to restore membrane excitability to normal.
Other options, but limited:
- HD (access limited)
- Insulin gtt with dextrose (15-45 min onset time)
- Lasix (5-15 min onset time)
What acid-base disorder is likely to occur with acute severe diarrhea?
Metabolic acidosis
- Diarrhea induces GI losses of bicarbonate
What are the most serious complications of hyperphosphatemia?
Metastatic and vascular calcification of non-skeletal tissues
Define metabolic alkalosis.
Characterized by an elevation in pH, an increase in [serum HCO3], and compensatory HYPOventilation, resulting in a RISE of PCO2
Common Causes:
- Loss of gastric acid (HCl) as a result of V or NG suction
- Loss of intravascular volume and chloride as a result of diuretic use
- Overzealous tx metabolic acidosis of bicarbonate OR an excess of acetate in PN solutions (which is metabolized to bicarb with a normally functioning liver)
- Some renal impairment must exist for this condition to occur
Tx: Treatment of the underlying cause; aggressive K repletion when hypokalemia is present in hyperaldosteronism
*
Define respiratory acidosis.
Characterized by reduced pH, an elevation in PCO2, and a variable increase in the [serum HCO3].
- Almost always results from a decreased effective alveolar ventilation, not an increase in CO2 production
Causes:
- Central depression of respiration
- Drugs (opioids, sedatives)
- Stroke
- Head injury
- Sleep apnea
- Airway or pulmonary abnormalities (airway obstruction, asthma, COPD, severe pulmonary edema, ARDS, pneumothorax, smoke inhalation)
- Neuromuscular abnormalities (Brainstem or cervical cord injury, Guillain-Barre syndrome), myasthenia gravis, MS)
- Obesity HYPOventilation
- Mech vent HYPOventilation
- PN/EN OVERfeeding
Define respiratory alkalosis:
Characterized by elevated pH, a decrease in PCO2, and a variable reduction in [serum HCO3]. Occurs when effective alveolar ventilation is increased beyond the level necessary to eliminate metabolically produced CO2.
Common Causes:
- Central simulation of respiration
- Anxiety, pain, fever
- Brain tumors
- Vascular accidents
- Head trauma
- Pregnancy
- Catecholamines, Salicylate toxicity
- Peripheral stimulation
- Pulmonary embolus
- Asthma
- High altitudes
- PNA
- Pulmonary edema
- Severe anemia
- Mech vent HYPERventilation
- Hepatic encephalopthy
Glycolysis occurs in the ____ state
Fed
The breakdown of glucose into pyruvate to produce energy
Glycolysis
End product of glycolysis
pyruvate
Endogenous formation of glucose from non carbohydrate sources
Gluconeogensis
What are common substrates for gluconeogenesis
fat, amino acids, lactic acid
What is the purpose of gluconeogenesis
to maintain plasma glucose during the fasted state and hypoglycemia
Where does gluconeogenesis occur
the liver , kidneys and small intestines
Gluconeogenesis occurs in the ___ state
fasted
Which counterregulatory hormones are involved in gluconeogensis
epinephrine, norepinephrine, cortisol, glucagon, thyroid hormone, growth hormone
what are the precursors for gluconeogenesis
lactic acid, alanine or glutamine amino acids and glycerol from broken down triglycerides
what is the preferred amino acid for gluconeogenesis
alanine (it converts into oxaloacetate from malate)
Gluconeogenesis will start within ____ ____ when there is no glucose
4-6 hours
How long until glycogen is depleted in a 70 kg male during starvation
24 hours
what are the fasting hormones (catabolic)
Glucagon, glycogenolytic, gluconeogenic, lipolytic and ketogenic hormones. Also released during stress and infection
Lipolysis
catabolism of the storage form of fat
Lipolysis happens during a ____ state
fasted state/ stress
Which hormone suppresses lipolysis
insulin
Lipolysis is triggered by the hormone ____ when blood glucose is ____
glucagon, low
Lipolysis is inhibited by the hormone ____ when blood glucose is ____
insulin, high
Branched Chain Amino Acids are stored in the ____state
Fed
which amino acid is used in gluconeogenesis
alanine
what is the role of amino acids in the kidney and brain
gluconeogenic amino acids that are made into glucose during gluconeogenesis. Works for the brain as neurotransmitters, pre-cursors to catecholamines etc.
an antioxidant derived from amino acids that plays a role in the development of arginine and nitrous oxide for preventing oxidative damage
glutathione
the primary substrate for gluconeogenesis in starvation
Protein
ketogenesis will start within ________ ______ during starvation
48 hours
Glucagon is released in response to _____ BG as well as _____ and _____
low blood glucose, stress, sepsis
Amino acid needed for transport and metabolism of long chain fatty acids into the matrix of the mitochondria for beta oxidation
carnitine
_____deficiency leads to impaired fatty acid oxidation which can increase the chance for hepatic steatosis
carnitine
Insensible water losses come from primarily the ____ and ___
skin and lungs
how long is the small intestine
350-600 centimeters
how much fluid does the duodenum secrete
9 liters (2 liters from PO, 7 liters of gastric fluid)
role of the ileocecal valve
Prevents backsplash of colon contents into the jejunum. Closes when there is an increase in colonic pressure
complications of ileocecal valve removal
decreased B12 absorption, decreased bile salt reabsorption, rapid GI movement of the small bowel contents into the colon which can cause malabsorption
______ are partially digested in the large bowel then consumed by gut bacteria where it is fermented and made into short chain fatty acids for energy for the colonocytes
soluble fiber
short chain fatty acids are derived from which type of fiber
soluble fiber
which type of fiber adds bulk to stool to soften it
insoluble fiber
conditions that cause gut dysbiosis
obesity, diabetes, IBD/IBS, cancer
where are sodium and water absorbed most efficiently
colon and ileum
where is fat primarily absorbed
duodenum / proximal jejunum
Primary absorption site of iron
duodenum
primary absorption site of manganese and folic acid
jejunum
Medium Chain Triglycerides are used during fat malabsorption because
they don’t have to be formed into micelles, they are water soluble and go right into circulation and don’t require bile salts.
Benefits of short chain fatty acids
inhibit cholesterol formation improve splanchnic circulation enhances immunity helper T cells inhibits pathogen growth decreases luminal pH lowers bile solubility
Primary absorption site of vitamin B 12
ileum
where are the majority of water, electrolytes and minerals absorbed
colon and small intestine
potassium and bicarobonate are secreted into the
colon
water follows sodium via this mechanism
osmosis
ileal or colonic losses from diarrhea or high output fistulas can lead to
hypokalemia, acidemia from loss of bicarbonate
most dietary iron is in the ______ form which is poorly absorbed in the gut
Ferric Fe2+
In order for iron to be absorbed, it has to change into the ______ form
Ferrous Fe3+
Which vitamin aids in the reduction of the Ferric Form (Fe2) of Iron to the Ferrous form (Fe3) of iron for easier absorption
Vitamin C (ascorbic acid)
What can be added to foods to enhance the absorption of iron in non-heme foods
Vitamin C
what amino acid provides the main fuel for enterocytes
glutamine
the absence of this amino acid can lead to mucosal atrophy
glutamine
site of primary protein digestion
duodenum
which enzymes digest protein
pepsin/pepsinogen when mixed with chyme
what amino acids are most rapidly absorbed
branched chain amino acids and essential amino acids
the primary energy source for the GI tract is ________ which has trophic effects and helps with immune function
glutamine
there is an increased need for what amino acid in critical illness
glutamine
what is the most abundant amino acid
glutamine
detriments of inadequate glutamine
GI mucosal atrophy, impaired immune function, increased risk for sepsis/bacterial translocation
which amino acids are important for the small intestine
glutamine and aspartate
what function do amino acids provide the liver
synthesis of plasma proteins: albumin, pre albumin, transferrin, clotting factors (fibrinogen/prothrombin)
The amino acid alanine is used for what in the liver
gluconeogenesis
Bile drains into the
duodenum
a disturbance of the lymphatic system in which fluid is incorrectly distributed and does NOT respond to diuretics
lymphedema
Recommended sodium dosage provides ___ to ___ mEq/kg of sodium
1-2 mEq/kg
normal serum sodium range
135-145
when serum sodium is low, cells are known as ______tonic
hypotonic
primary sodium losses occur from
NGT suction, fistula drainage, adrenal insufficiency
when there are increased solutes in the blood circulation, water shifts from inside of the cell to outside of the the cell resulting in which type of hyponatremia
hypertonic hyponatremia
Primary IV treatment of hypovolemic hyponatremia
normal saline
Causes of hypovolemic hyponatremia
Third Spacing (SBO, low albumin)
Diarrhea, Vomiting, NGT suction (GI losses)
Diuretics
primary treatment of hypervolemic hyponatremia
Water restriction
causes of hypervolemic hyponatremia
CHF, Cirrhosis, TURP
primary treatment of isovolemic hyponatremia
water restriction
causes of isovolemic hyponatremia
too much IVF, water intoxication, diuretics, SIADH, drugs
the hormone released by the pituitary gland that tells your kidney how much water to conserve to maintain blood pressure by concentrating the urine
Anti Diuretic Hormone
When your body has high levels of ADH, the kidneys re-absorb too much water. Total body water will increase and becomes hypo-osmolar and sodium decreases which is known as
SIADH (symptom on inappropriate diuretic hormone)
Etiologies of SIADH
malignant tumors, head trauma, meningitis, schizophrenia meds, post surgical
Treatment for SIADH
water restriction , sodium supplementation
Acute hypotonic hyponatremia (acute water intoxication)
Sodium <125mEq/L causing headache, nausea, confusion. Na <110 mEq/L can cause seizure, coma or death
Sodium Deficit Calculation
Normal Na - Current Na x body weight in kg x % body water
Give no more than ___ free water deficit a day or > mEq/day when restricting sodium
1/2 of the free water deficit or 6-12 mEq/Day
a condition of cerebral edema (which can be deadly) in which too much sodium is given too much at one time is known as
osmotic myelinolysis
Hypertonic saline (3%) is used to treat
severe hyponatremia when a patient is confused or obtunded
when giving hypertonic saline, serum Na should be checked how often
every 1-2 hours
Don’t correct Na more than ____ to ____ a day
6-12 mEq/day
How much sodium would you replete for a 70kg male with a serum sodium of 120mEq/L with headache and confusion
126-120 x .6 x 70 kg = 252 mEq sodium
symptoms of hypernatremia
lethargy, confusion, twitching , stupor, coma
failure of the central brain to release ADH or failure of the kidneys to respond to ADH is known as
Diabetes Insipidus
Symptoms of diabetes insipidus
polyuria, polydypsia,hypernatremia , retained sodium
is sodium high or low in diabetes insipidus
high
treatment of diabetes insipidus
hypotonic fluids 0.2 or 0.45% NaCl, volume restriction, sodium restriction
the major intracellular electrolyte
potassium
normal serum range of potassium
3.5-5
typical IV dose of potassium ins mEq/kg/day
1-2 mEq/kg/day
causes of hyperkalemia
acidosis (Hydrogen moves out of the blood to become less acidic and into the cell, so potassium will move out of the cell into the blood), renal failure, traumatic blood draw (false positive), hemolysis, burns, crushing syndrome, NSAIDS, K sparing diuretics, tacrolimus
symptoms of hyperkalemia
EKG changes, decreased heart rate, arrthymias, high T waves, wide QRS, heart block, atrial systole, cardiac arrest, muscle cramping/twitching, weakness
What is the first step of potassium correction to stabilize the heart
calcium gluconate
What is the second step of potassium correction to shift potassium back into the cell
sodium bicarb, 100mL 50% dextrose, 10 units of insulin
Other methods to reduce potassium in hyperkalemia after calcium gluconate and correction of acidosis
dc or decrease supplemental potassium, use K sparing diuretics like Lasix, dialysis
symptoms of hypokalemia
weakness, lethargy, constipation, arrhythmia, psychosis, post op ileus, flat T waves
causes of hypokalemia
diarrhea, high urine output, metabolic alkalosis, increased amounts of insulin, catecholamines, furosemide, thiazide diuretics, sorbitol, refeeding syndrome
IV forms of potassium
potassium chloride, potassium acetate, potassium phosphorous
what type of potassium is preferred in acidosis
potassium acetate
potassium takes ___ hours to normalize
2 hours
Avoid providing IV potassium with ______ as glucose/insulin will increase forcing potassium into the cell and worsen hypokalemia
dextrose
you must correct ______ to correct potassium
magnesium
normal serum mangesium
1.8-2.8
magnesium is primarily absorbed in the
jejunum/ileum
magnesium is primarily excreted by the
kidneys
symptoms of hypomagnesemia
low potassium, tetany, decreased insulin sensitivity, arrhythmias
causes of hypomagnesemia
refeeding syndrome, decreased intake/absorption, prolonged magnesium free PN, alcoholism, ileostomy, short bowel syndrome, loop diuretics, DKA
what route of magnesium replacement is preferred
IV, oral can cause GI upset
max infusion rate of magnesium
1 gram per hour (less in renal failure)
replace magnesium with ____ in order to decrease risk of cardiac arrhythmias
potassium
causes of hypermagnesemia
chronic kidney disease and high magnesium intake/provision in EN/PN
symptoms of hypermagnesemia
nausea, diaphoresis, flushing/heat flash, bradycardia, hypotension
IV treatment for hypermagnesemia
calcium chloride or calcium gluconate
medication treatment for hypermagnesemia
loop diuretics
normal calcium range
8.6-10.2
what hormones control calcium
parathyroid hormone, vitamin D and calcitonin
the release of PTH is signaled by low _____ to increase _________, __________ and _________
calcium ; bone resorption, renal conservation, absorption in the gut
Vitamin D increases calcium by
increasing gut absorption of calcium
Calcitonin is signaled by ________ calcium to ______ osteoclast function
high calcium to decrease osteoclast formation to stop releasing calcium
Ionized Calcium normal range
1.2-1.3 mmol/L
what is the most accurate way to measure serum calcium
ionized calcium
ionized calcium is not affected by _____-
albumin
Calcium correction for hypoalbuminemia
4- serum albumin x .8 + serum calcium
etiologies of hypocalcemia
low albumin, decreased vitamin D activity, hyperphosphatemia, decreased PTH, hypomagnesemia, citrate anticoagulation in CRRT, thyroidectomy, sepsis, rhabdomyolysis, blood transfusion, bisphosphonates, furosemide, calcitonin, phenytoin
symptoms of hypocalcemia
decreased blood pressure, decreased myocardial contraction, decreased QT prolongation, extremity parenthesis, cramps, tetany
preferred IV fluid to correct hypocalcemia
calcium gluconate or calcium chloride
provide ____ to aid in calcium correction
magnesium
oral forms of calcium repletion
calcium acetate, vitamin D supplements, calcium citrate, calcium carbonate (tums)
causes of hypercalcemia
cancer, hyperparathyroidism, high vitamin D or A intake, chronic intake of milk, antacids or calcium supplements, lithium, TB, thiazide diuretics
symptoms of hypercalcemia
fatigue, nausea, vomiting, constipation, anorexia, cardiac arrhythmia, bradycardia
treatment of mild hypercalcemia
hydration and ambulation
treatment of hypercalcemia in setting of malignancy
bisphosphonates
treatment of severe hypocalcemia
lasix, hemodialysis, 1,000-1,500 mg elemental calcium, IV calcium chloride or calcium gluconate
normal range of phosphorous
2.7-4.5
functions of phosphorous
makes up bone, pH balance, makes up ATP, carbohydrate metabolism, part of 2.3-diphosphoglycerate on RBCs, muscle function, myocardial function and all cell function
regulation of phosphorous
intestinal absorption, renal excretion, hormone regulation, bone resorption (deposition)
causes of phosphorous shifts
carbohydrate/insulin, catecholamines and alkalosis
symptoms of hypophosphorous
ataxia, confusion, paresthesia, hemolysis, refeeding syndrome
etiologies of low phosphorous
alcoholism, critical illness, respiratory or metabolic acidosis, DKA treatment 2/2 insulin, high CHO in TPN especially if malnourished
treatment of mild hypophosphorous
K Phos, Phos NaK
treatment of symptomatic hypo phosphorous
IV K phos or IV Na Phos
____mmol of phos = 4.4 mEq potassium
3
causes of hyperphosphatemia
CKD, ESRD, trauma, hemolysis, rhabdomyolysis, respiratory metabolic acidosis, high dose phos containing enemas
If a patient has excessive vomiting with bile they will have low
sodium and chloride
gastric juice contains ____ to ___ mEq/L of chloride
120-160 mEq chloride
bile contains ______ to ______ of sodium
120-170 mEq/L
diarrhea contains _____ to _____ mEq/L of potassium
10-60
if a patient has excessive diarrhea, they will be low in
potassium and sodium (and zinc!)
if a patient has large volumes of NGT suction what could you expect in regards to electrolyte/acid base balance
decreased chloride, decreased sodium and metabolic alkalosis
composition of lactated ringers
130 mEq sodium, 4 mEq potassium, 3 mEq calcium, 109 meQ chloride, 28 meQ bicarb will transform into acetate, lactate , 280 osmoles
which IV fluid is compositionally comparable to the jejunum
lactated ringers
composition of normal saline
154 mEq sodium 154 mEq chloride , 308 milliosmoles
composition of D5W
Dextrose 5% per liter, water, 250 mOsm
which IV fluid has the lowest osmolarity
D5W
D5W + 0.45 NaCl
Dextrose, Water, 77 mEq sodium 77 mEq chloride, 405 milliosmoles
which IVF has the highest osmolarity
D5W with 1/2 normal saline (0.45NaCl) with Potassium
where are 90-95% of bile salts re absorbed
terminal ileum
water and sodium are most efficiently absorbed here
ileum and colon
catabolism of this macronutrient is most common in stress starvation
Fat (lypolysis)
the gallbladder is stimulated by
cholecystekinin
high insulin levels suppresses this form of metabolism
lipolysis (insulin increase indicates fed state)
which enzyme starts the digestive process of carbs in the mouth
salivary amylase
homeostasis of copper is driven by
excretion
the majority of copper is absorbed by the
duodenum
phytates, zinc, iron and large vitamin C doses interfere with ___ absorption
copper
copper is excreted via
bile
oxidation/reduction reactions, electron transfer, manganese oxidation glucose metabolism, and oxidation of ferrous to ferric form of iron are roles of
copper
Copper deficiency inhibits ______ absorption
iron
deficiency of copper causes _____ deficiency
iron deficiency anemia
Iron needs to be reduced to the ferric state so it can bind to transferrin on the red blood cell. This is inhibited by ____ deficiency leading to iron deficiency anemia
copper
copper deficiency causes _____ ____ anemia (type of RBC)
microcytic , hypochromic
populations at risk for copper deficiency
bariatric surgery, intestinal surgery, diarrhea, malabsorptive disorders
excessive copper can be secondary to _____ excretion leading to oxidative damage
impaired gallbladder (biliary)
Wilson’s disease is caused by excess ______ in the liver, typically causing liver cirrhosis
copper
hypopigmentation of the hair, Kayser Fleisher rings in the eyes, hypochromic microcytic anemia are symptoms of ____ deficiency
copper
an overdose in zinc causes ______ deficiency
copper
_____ medications decrease copper absorption
acid reducers as copper digestion relies on HCL From the stomach
Copper deficiency is common in ______ disease and requires supplementation when anemic
Celiac disease
Copper overload occurs with
parenteral nutrition 2/2 limited gall bladder stimulation for excretion
manganese is excreted by the
bile
this mineral is involved in the make up of metalloenzymes, arginase and pyruvate carboxylase
manganese
populations at risk for manganese toxicity
long term TPN
irritability, hallucinations, ataxia, and hepatic damage, Parkinson’s like symptoms, altered gait are all sings/symptoms of _____ toxicity
manganese
the content of this mineral in food depends on soil levels
selenium
thyroid alterations can occur in long term PN with out _____ supplementation
selenium
hair/nail loss, peripheral neuropathy, tooth decay and fatigue can be symptoms of ___ toxicity
selenium
selenium deficiency also concurs with ____ deficiency limiting thyroid function
iodine
this micronutrient is taken up by the thyroid to synthesize thyroid hormones
iodinne
what is the metabolically active form of thyroid hormone
T3
goiters are symptoms of ___ deficiency
iodine
increased TSH and depressed thyroid activity are results of ____ deficiency
iodine
iodine isn’t available in PN formulations. The alternative method to provide iodine in long term PN patients is
antiseptic preparations on the skin
this micronutrient is essential for glucose and lipid metabolism by mobilizing insulin
chromium
hyperglycemia is a symptom of ____ deficiency (trace mineral)
chormium
fluoride is primarily absorbed in the
stomach
functions of fluoride include
bone mineralization, hardening of tooth enamel, protects calcified tissues from demineralization, inhibits dental carries
teeth mottling, nausea/vomiting/diarrhea are all symptoms of ____ toxicity
fluoride
absorption of molybdenum occurs in
the stomach
molybedenum are excreted via the
kidneys
ultra trace elements (lead, lithium, nickel, tin etc) are elements needed in less than _____ mg /day and have no ____ or _____ determined
RDA or AI’s
now that vitamin K is added to the PN MVI, take caution with patients on this medication
Coumadin/Warfarin (monitor INR)
Parenteral trace elements
selenium, copper, manganese
in the setting of parenteral MVI/Trace element shortages, what is recommended
prioritize the most vulnerable
a patient with mental status changes (dementia) , dermatitis and diarrhea may have this deficiency
niacin deficiency (Pellagra)
manganese toxicity is common in long term PN because its route of excretion is
the gallbladder/bile
_____ toxicity occurs with cholestasis (a long term complication of PN)
manganese
extrapyramidal symptoms such as Parkinson’s like symptoms, muscle ridgitiy and tremors, and altered gait are symptoms of ____ toxicity
manganese
the most common micronutrient toxicity in long term PN regardless of liver function is
hypermanganese
if a patient exhibits cholestasis, limit these elements by providing ___ and ___ free trace elements in long term PN patients
manganese, copper
supplementation of this element may help reduce hyperglycemia
chromium
patients with significant GI losses including diarrhea are at risk for deficiency of this element
zinc
in wounds, high ostomy output and excessive diarrhea supplement with this element
zinc
serum zinc is not a reliable marker of zinc status because
it is bound to albumin which is widely available in the body
zinc and copper will not compete for absorption in
IV doses in PN
Case: A patient who is PN dependent with a daily output of 3L from his ileostomy, has recently increased BUN/Creatinine ration and a serum sodium of 131 mEq/L is at risk for what deficiencies. The increased BUN/Cr ratio is likely 2/2 ______. Hyponatremia is likely 2/2 ____ losses when fluid replacement doesn’t contain adequate NA. ______ supplementation is recommended to prevent deficiency as there is likely high losses from the ileostomy drainage
water, sodium,zinc
dehydration
GI losses
Zinc
headaches and Parkinson’s like activity (extrapyramidal symptoms) are a result of ____ toxicity
manganese (sometimes zinc)
if a patient with short bowel syndrome who has required PN for 2 years presents with dysgeusia, diarrhea and alopecia, they most likely are deficient in
zinc
What are the monosaccharides?
Glucose, galactose, fructose
Name 3 common disaccharides
Sucrose (1 glucose and 1 fructose)
Maltose (2 glucose moieties)
Lactose (1 glucose and 1 galactose)
Are complex carbs water soluble or insoluble?
Insoluble with high molecular weights.
What are oligosaccharides?
Polysaccharides containing fewer than 10 glucose units
What are the straight chains in starch called?
Amylose
What are the branched chains in starch called?
Amylopectin
How do glucose and galactose enter enterocytes?
Through sodium-glucose transporter 1 (SGLT1), an adenosine triphosphate (ATP)-dependent active transporter
Which protein transports fructose?
GLUT5 (glucose transporter 5)
What are the 2 classes of glucose transport proteins?
The sodium dependent glucose transporters and the facilitative transporters
Describe the function of facilitative transporters
Function as passive diffusions channels (channels dependent on the gradient of glucose concentration between extra- and intracellular compartments) and do not require sodium or ATP. Present in many different tissues
Describe the function of sodium dependent glucose transporters
Involved in the active, ATP-dependent absorption of glucose from the intestinal lumen into cells. Also function in the reabsorption of filtered glucose in the proximal tubule of the kidney
Where are the highest concentrations of GLUT1?
Endothelial (major part of the blood-brain barrier) and glial cells of the brain
Which monosaccharides are transported by GLUT1?
Glucose and galactose
Where is GLUT2 mainly located?
Liver, small intestine, and kidneys
Describe the action of GLUT2 in the liver (1), kidneys (2), small intestine (3)
- In hepatocytes, GLUT2 has a low affinity but high capacity for glucose, allowing quick equilibration of intracellular and extracellular glucose concentrations across the membrane during fasting and fed states.
- GLUT2 transports the reabsorbed glucose back into the bloodstream from proximal tubular epithelia.
- GLUT2 is important in the transepithelial transport of the absorbed glucose
Where is the highest concentration of GLUT3?
The neuronal membranes of the brain
Describe the action of GLUT3 in neuronal cells
Controls the rate of glucose entry into neuronal cells
Where is GLUT4 mainly located?
Adipose (brown and white) and muscle (skeletal and cardiac) tissues. Mainly within the intracellular vesicles of these tissues but can be translocated to the cell surface in response to a rise in plasma insulin concentrations or muscle contraction
Where is GLUT5 mainly located?
The apical membrane of the jejunum
What is the formula that expresses the net chemical reaction of glucose catabolism?
C6H12O2 + 6O2 –> 6CO2 + 6H2O + Energy
Where in the cell does glycolysis take place?
The cytoplasm
Where in the cell does the TCA cycle take place?
Inside mitochondria
Glucose absorption into which organs is dependent on insulin? Independent?
Skeletal muscle and adipose tissue glucose absorption is insulin dependent.
Liver, kidney, brain, other tissue glucose absorption is insulin independent.
Name the substrates and major sites of expression for GLUT1
Substrates are glucose, galactose, mannose, and glucosamine
Major sites of expression are erythrocytes, CNS, blood-brain barrier, placenta, fetal tissues in general
Name the substrates and major sites of expression for GLUT2
Substrates are glucose, galactose, fructose, mannose, glucosamine
Major sites of expression are liver, beta-cells of pancreas, kidney, small intestine
Name the substrates and major sites of expression for GLUT3
Substrates are glucose, galactose, mannose, xylose, dehydroascorbic acid
Major sites of expression are brain (neurons), spermatozoa, placenta, preimplantation embryos
Name the substrates and major sites of expression for insulin dependent GLUT4
Substrates are glucose, glucosamine, dehydroascorbic acid
Major sites of expression are muscle, heart, brown and white adipocytes
Name the substrates and major sites of expression for GLUT5
Substrates are fructose, but not glucose
Major sites of expression are intestine, kidney, brain, skeletal muscle, adipose tissue
The net chemical reaction of glucose catabolism results in:
An equal number of moles of CO2 and oxygen, creating a respiratory quotient of 1
Glycosis converts glucose into:
Pyruvate
Where does the glycolytic pathway in the cell take place?
Cytoplasm
Approximately __ kcals are released per mole of ATP
7
What are the 3 major enzymes in glycolysis?
Glucokinase, phosphofructokinase, and pyruvate kinase
Where in the cell does the TCA cycle occur?
Mitochondria, only under aerobic conditions
What is the metabolic reaction of cell respiration?
The TCA cycle
Using the pyruvate-lactate pathway, how many ATPs can be generated per molecule of pyruvate?
2
The oxidation of 1 glucose molecule produces __ molecules of ATP total from which 2 types of reactions?
36 molecules of ATP. 4 molecules via substrate phosphorylation (2 from glycolysis and 2 from pyruvate decarboxylation) and 32 molecules via oxidative phosphorylation
Which pathway allows some organisms to survive under anaerobic conditions?
Pyruvate-lactate pathway
What are the 4 distinctive, irreversible reactions of gluconeogensis?
- Pyruvate is carboxylated in mitochondria to oxaloacetate
- The formed oxaloacetate is phosphorylated in the cytosol to phosphoenolpyruvate
- Special phosphatases hydrolyze fructose 1,6-biphosphate
- Special phosphatases hydrolyze glucose 6-phosphate
When can amino acids and fat provide carbon for gluconeogenesis?
During fasting or carbohydrate deprivation
What is the purpose of gluconeogenesis?
It is the endogenous formation of glucose and is important to maintain plasma glucose concentration in the normal range during fasting and allows constant provision of energy for metabolic needs
The body stores carbohydrate as:
Glycogen
In a 70 kg healthy person, the liver contains approximately __ gm of glycogen
100 gm (has the potential to provide 390 kcal)
Skeletal muscle contains about ___ gm of glycogen which suggests that an adult has enough glycogen to last for how long while performing normal activities?
Contains 300-400 gm glycogen, yielding less than 1560 kcal, suggesting that an adult stores enough glycogen for about a day of normal activities
The formation of glycogen is called ___, and the breakdown of glycogen is called ___
Glycogenesis
Glycogenolysis
Glycogen synthesis and glycogenolysis are regulated by the rate-limiting enzymes:
Glycogen synthase and glycogen phosphorylase, respectively
What are the primary substrates to gluconeogensis?
Lactate, glutamine, alanine, and glycerol
After 14 days of fasting, adipose tissue can provide more than what percent of daily energy requirements?
90%
After how many weeks of starvation is the brain able to adapt to using ketones as a source of energy?
1-2 weeks
Describe how stress hyperglycemia occurs?
During periods of trauma and illness, there is increased production of stress hormones such as epinephrine and cortisol, accompanied by an elevation in growth hormone and glucagon. These counterregulatory hormones oppose insulin action, causing increased glucose production by the liver (may exceed 500 gm glucose per day) and decreased utilization of glucose in peripheral tissues. Acute and chronic disease and injury can also increase production of cytokines which further contribute to hyperglycemia through stimulation of counterregulatory hormone release and suppression of insulin action
How can gastric emptying be delayed in regard to fiber intake?
Increased viscosity of gastric contents, which reduces pyloric flow
A minimum of __ gm of carbohydrates per day is required to avoid ketone production
50 gm
During moderate exercise, approximately __% of energy is provided by glucose
60%
What should be done if a pregnant patient with gestational diabetes loses weight?
If patient’s response to diagnosis of gestational diabetes is to self-starvation to avoid hyperglycemia, test urine for ketones and increase carb intake
Describe direct calorimetry and how it is performed
Measures heat and chemical energy released from the body. Heat is considered a direct measurement of metabolic rate because the fuel energy used by the body is ultimately transformed to heat. Urine also is collected to account for the small amount of chemical energy lost in urea excretion in urine. These machines consist of a living space or chamber thermally isolated from the outside, with equipment to extract and measure the heat released into the air of the chamber from the subject residing within. Most appropriate in the study of healthy subjects in research/academic environments due to the individual needing to remain alone in the chamber without caregivers or medical equipment. Can last for days.
Describe indirect calorimetry and how it is performed
Gas exchange and heat measurements are obtained simultaneously and are used to deduce the ratios of gas exchange to head production and prove the equivalence pf the 2 processes. The measurement of gas exchange is shown to be an indirect but accurate reflection of energy expenditure. Subjects do not need to be isolated as long as respiratory gases can be completely captured for approximately 30 minutes. Most IC devices consist of sensors for measuring oxygen and CO2 concentrations in inspired and expired air, a device for measuring exhaled minute volume, and a computer system to calculate parameters and manage data.
What is the Reverse Fick Equation?
An estimation of oxygen consumption, derived from oxygen content differences in arterial and mixed venous blood multiplied by cardiac output measurements from pulmonary artery catheters. Not useful for clinical assessment of energy expenditure
What is the Doubly Labeled Water technique?
A method for assessing energy expenditure that involves administering a stable isotope of water (2H2O) to the patient and measuring its disappearance rate over time (days). The disappearance of 2H is proportional to water turnover, whereas the disappearance of 18O is proportional to water turnover plus VCO2 production. The difference between the 2 disappearance rates is the VCO2. VO2 is computed from the food quotient (FQ - the sum of the CO2 produced from all food eaten divided by the sum of the oxygen consumed during oxidation of all food eaten). Useful for research, not used in clinical care.
Name the relative indications for Indirect Calorimetry
BMI <20.5
BMI >80
Concern about overfeeding in a patient with unexplained high ventilator requirement or who for an unknown reason cannot be liberated from the ventilator
Unwanted weight loss over time not explained by volume status in a patient who regularly receives nearly 100% of target feeding
Massive tissue loss from amputation
Preadmission fluid overload (ascites, volume resuscitation, “third spacing”) without a reliable report of body weight at proper hydration
What are the contraindications for Indirect Calorimetry?
Air leak (chest tubes, cuff leak, any other leak in ventilator circuit, leaks around face masks, canopies, etc.)
ECMO
HD (during and for several hours afterwards)
For mechanically vented patients, a fraction of inspired oxygen >60%
For spontaneously breathing patients:
- Reliance on any supplemental oxygen (cannula, face mask, etc.)
- Inability to cooperate with the measurement
- Claustrophobia or any anxiety about the measurement
What is the amount of time that IC measurements are useful for in critically ill, mechanically ventilated patients?
3-4 days
What is the maximum BMI that was used when the Mifflin - St. Jeor equation was being studied?
Maximum BMI of 42
How is the accuracy rate of the Mifflin-St. Jeor equation affected when applied to obese people?
It falls somewhat. Accuracy of 75% in people with BMI 30 or higher, compared to 87% in people with BMI less than 30
What are the 2 earliest and most common ways to predict RMR in critically ill patients?
Using a ratio of kcal to kg of body weight OR calculate healthy RMR (with Harris-Benedict or Mifflin-St. Jeor) and multiply by a stress factor.
In which populations has the Penn State Equation been demonstrated to be accurate?
Morbidly obese (80% accuracy up to a BMI of at least 80)
Brain injuries (72% accuracy)
Barbiturate coma (73% accuracy)
In which populations does the Penn State Equation lose accuracy?
Low BMI (63% accuracy when BMI is <20.5)
Cystic fibrosis (58% accuracy; many of these patients had very low BMI which might be the underlying reason for the low accuracy rate)
VCO2 stands for:
Volume of CO2 production
VCO2 is calculated as:
The breath-by-breath exhaled volume multiplied by the fraction of expired CO2, averaged over a minute, and then aggregated to a 24-hour period
VO2 stands for:
Oxygen consumption
VO2 calculation:
VO2 = VCO2/RQ
VO2 is calculated from the algebraic manipulation of the RQ (respiratory quotient) equation and combined with the Weir equation to calculate RMR
What is the equation for RMR measurement (kcal/day) using ventilator-derived measurement of CO2 production?
VO2 = VCO2/RQ
where RQ is calculated from the actual fuel intake, or assumed to be approximately 0.85
RMR = (VO2 x 3.91) + (VCO2 x 1.1) + 144
where RMR is measured in kcal/day, and VO2 and VCO2 are measured in mL/min
Show the modified Weir equation (used with VO2 and VCO2 to interpret IC data)
RMR = [(VO2 x 3.94) + (VCO2 x 1.1)] x 1.44
What is the metabolic range of RQ?
0.67 to 1.3
Show the Mifflin-St. Jeor equation
Men: RMR = 5 + (10 x W) + (6.25 x H) - (5 x A)
Women: RMR = -161 + (10 x W) + (6.25 x H) - (5 x A)
where RMR is measured in kcal/day, W is weight in kg, H is height in cm, and A is age in years
Show the Penn State equation
RMR = (Mifflin-St. Jeor x 0.96) + (Ve x 32) + (Tmax x 167) - 6212
where RMR and MSJ are measured in kcal/day, Tmax is the maximum body temp in the previous 24 hours (celsius) and Ve is minute ventilation in L/min
What are the 3 major components of total energy expenditure (TEE)?
- Basal metabolic rate (BMR) or resting metabolic rate (RMR)
- Energy required for thermogenic effect of digestion
- Energy expenditure associated with physical activity
What is the difference between BMR and RMR?
BMR is metabolic rate measured in a fasting state, immediately upon awakening and before any physical activity is undertaken. RMR is also measured in a fasted state, but some movement is allowed before testing (dressing, walking)
What are the influences on RMR?
Determined by body size and composition, sex, and age. Some sex and age effects are indirect, being the result of the amount or composition of the fat-free mass rather than related to biological sex differences or age.
Name the numerous factors that seem to influence the thermogenic effect of digestion
Diet factors (size and composition of the meal, time of day the meal is eaten), age, smoking, stress, caffeine use.
True or false: The thermogenic effect of digestion is induced in healthy people who are being fed with a continuous infusion of liquid formula via gastric feeding tube.
False. It is NOT induced.
How does tissue synthesis in nutrition repletion, pregnancy, and childhood increase energy requirements?
Tissue synthesis is a high-energy activity. The newly synthesized tissue is composed of fuel (protein and fat), and the synthesis of new tissue from individual amino acids, fatty acids, and glucose is an energy-requiring reaction.
A study found that differences in RMR of trauma, surgical, and medical critical care patients were eliminated when which factor was controlled?
Temperature.
The length of time before bodily function compromise occurs after energy needs are not being met depends on:
The patient’s nutrition status, the size of the energy deficit, the body compartment being catabolized
In what conditions will a critical deficit in energy be reached sooner?
Malnourished patients (they start with a reduced tissue reserve), hypermetabolic patients (they create larger daily deficits), and in cases where inflammatory response favors catabolism of protein over fat
Which particular fatty acids are critically important to proper development as well as inflammatory and other physiological processes?
Arachidonic acid, eicosapentaenoic acid (EPA), and docohexaenoic acid (DHA)
What are the basic contents of triglyceride structure?
A glycerol backbone and various fatty acids attached in ester linkage at the carbon-1 (sn-1), carbon-2 (sn-2), and carbon-3 (sn-3) positions
Why does a gram of fat stored in tissue have more recoverable energy than a gram of carbohydrate?
TGs have a lower intrinsic level of oxidation than carb, and the weight contribution of water common to carbs and proteins is missing from lipids
Which fatty acids necessary for life can humans not synthesize and why?
Linoleic acid and alpha-linolenic acid. The specific desaturase enzymes that can introduce a doube bond past position 9-10 within a given fatty acid are absent, which prevents the de novo synthesis of linoleic and alpha-linoleic acids.
Linoleic acid and alpha-linolenic acid serve as precursors for the synthesis of which other necessary long-chain unsaturated fatty acids?
Arachidonic acid (AA) and docohexaenoic acid (DHA)
What is the intestinal activity that is critical for metabolism of long-chain TGs?
The emulsification process and micelle formation that makes TGs and fatty acid esters available for hydrolysis by intestinal lipases and esterases
What types of fats can be directly absorbed in the villi of the intestinal mucosa?
Ingested glycerol and individual fatty acids. MCT (medium-chain triglycerides) lipid emulsions can be directly absorbed without requiring either bile salts for emulsification or energy for uptake
What are ILEs (lipid injectable emulsion), and what concentrations are available in commercial ILEs?
Oil-in-water emulsions consisting of 1 or more TG-containing oils, glycerin, and a phospholipid emulsifier, available in concentration of 10%, 20%, and 30% (w/v).
How can hypertriglyceridemia occur with the provision of lipids in PN?
It occurs when the body cannot clear TGs from plasma lipids via oxidation and/or storage in adipose tissue, and it may be caused when the supply of lipids into the bloodstream exceeds lipoprotein lipase activity or when lipoprotein activity is reduced
What is the most common pathway of oxidative degradation of fatty acids?
Beta-oxidation
What is the suggested % of total energy as linoleic acid and alpha-linolenic acid that should be provided to prevent essential fatty acid deficiency (EFAD)?
1-4% for linoleic acid
0.25-0.5% for alpha-linolenic acid
The two 100% soybean oil-based emulsions available for IV use in the US provide what percent of total energy from linoleic and alpha-linolenic acid?
55-60% of energy from linoleic acid and 3-4% total energy from alpha-linolenic acid
What is the most common lipid regimen in adult PN patients with 100% soybean oil-based ILEs that is prescribed to meet EFA requirements?
500 ml of a 20% ILE may be given weekly
ASPEN guideline when using soybean oil emulsion as the sole IV fat sourse?
The ILE should be held for the first week or given at a maximum of 100 g/week if there is concern or risk for EFAD
In adult patients requiring PN, ILEs should not exceed ___ g lipid per kg per day
2.5 g
It is recommended that the infusion rate for ILEs does not exceed ___ gm/kg/hour, for what reason?
Recommended to limit the infusion rate so it does not exceed 0.11 gm/kg/hour to prevent potential adverse reactions or toxicities associated with rapid infusion
What strategies can prevent adverse metabolic outcomes when propofol is used concomitantly with nutrition support?
Clinicians should monitor serum TG concentration frequently (twice per week).
To lower the total fat dose and possibly improve TF clearance, lipids should be removed from PN solutions.
Recommendations for acceptable TG levels are <250 mg/dL 4 hours after ILE infusion for “piggy backed” lipids and <400 mg/dL for continuous ILE infusion.
Patient could be started on a hypocaloric, fat-free PN (=/< 20 kcal/kg/day) (if failed trophic EN).
What are the biochemical and clinical manifestations of EFAD (that were observed in patients requiring PN for extended periods of time [2-4 weeks])?
Clinical symptoms: increased susceptibility to infection, impaired wound healing, and immune dysfunction
Biochemical changes in response to linoleic acid deficiency are manifested by a decrease in linoleic acid and AA levels and an increase in the mead acid level (mead acid primarily produced in humans in the absence of EFAs)
Triene:tetraene ratio > 0.2
Why might EFAD occur rapidly in patients receiving fat-free PN administration?
Due to elevated insulin levels that prevent adipose tissue lipolysis.
Why might the period of time be extended before a patient exhibits EFAD when receiving hypocaloric fat-free PN or a cyclic feeding schedule of fat-free PN?
It is thought that when PN is cycled or hypocaloric PN Is provided, essential fatty acids are mobilized and enter the circulation as a result of increased lipolysis of endogenous fat stores in response to a reduction in serum insulin concentration. In addition, hypocaloric feeding prevents the risk of hepatic dysfunction that may occur if the energy deficit (caused by the removal of lipids) is corrected by increasing the energy from dextrose or protein to maintain energy requirements
How can essential fatty acid deficiency (EFAD) be prevented when a lipid-free PN regimen is initiated in the ICU?
Patients should be monitored for EFAD if all sources of lipids are removed from the diet for more than 2-4 weeks. The dosing of ILEs depends on energy expenditure, the patient’s clinical status, body weight, tolerance, and ability to metabolize lipids. Providing 2-4% of energy requirement as linoleic acid may correct EFA insufficiency. Should calculate the linoleic acid dose from 100% soybean ILE or an alternative ILE to ensure adequate dosing of EFAs. Initiation of low dose or trophic EN may also be used to offset risk of EFAD. A polymeric enteral formula containing soybean oil and a mixture of other high-linoleic oils may be used. Generally, a polymeric enteral formula that provides 10-15% of patient’s total energy requirements will supply adequate EFAs. However, when the patient is at high risk for fat malabsorption, or when enteral feeding is interrupted or stopped for a significant period (14 days) with no other lipid source provided, the linoleic acid dose and EFAD risk should be evaluated
What is the ASPEN recommendation regarding the use of immune modulating formulations in critical illness?
Immune-modulating enteral formulations of arginine with other agents - including EPA, DHA, glutamine, and nucleic acid - should not be used routinely in medical ICU. These formulas and similar ones (eg, fish oil with or without arginine) should not be administered to severely septic patients
Under which conditions does ASPEN recommend formulations that contain fish oil and arginine be considered?
Severe trauma and TBI
What is the primary source of SCFAs?
The large intestine via bacterial anaerobic fermentation of nondigestible dietary carbohydrates and fiber polysaccharides.
Fermentation of nondigestible carbohydrates and fiber polysaccharides produces which SCFAs?
Acetate, propionate, butyrate
Name some of the functions of SCFAs
A primary energy source for colonocytes, stimulation of water and sodium absorption in the colon, and trophic effects to the intestinal mucosa.
Which SCFA has been shown to be the most important in regulation and maintenance of colonic tissue and why?
Butyrate. An important role may be to modify inflammatory activity by inhibiting the release of the transcription factor, nuclear factor lambda-light-chain-enhancer, of activated B cells. Exhibits antitumorigenic effects on cancer cell lines and has been identified with gene regulation involving processes of cellular apoptosis, proliferation, and differentiation
Describe some differences between long-chain triglycerides and medium-chain triglycerides
MCTs are smaller and more water soluble, liberation of fatty acids through hydrolysis of MCTs in the intestinal lumen is significantly faster relative to LCTs, absorption of MCFAs is more rapid. MCTs do not require the presence of bile or pancreatic lipases for absorption and are transported directly to the liver via the portal vein. MCTs not stored to any significant degree in adipose tissue, nor do they affect reticuloendothelial system. MCTs are ketogenic, and may provide a useful energy source for enterocytes, lymphocytes, and cells of other tissues in hypermetabolically stressed patients. Oxygenation of MCTs is less affected by glucose and insulin than LCTs. Oxidation of LCTs can be impaired by slow elimination rates from the plasma or by the requirement of carnitine for intracellular transport; metabolism of MCTs is a carnitine-independent system for transport into the mitochondria.
What is the energy density of MCTs?
8.3 kcal/g
What are structured lipids?
“Designer” TG molecules that are specifically synthesized in the lab via chemical and/or enzymatic methodology or via genetic engineering. These TG mixtures contain a randomly esterified pattern of MCTs and LCTs that can contain within the same TG molecule both MCFAs and LCFAs
What are some benefits of a structured lipid?
Offer a defined mechanism to rapidly deliver MCFAs and to provide a more rapid availability of EPA and DHA with the entire attendant array of nutritionally positive aspects of these substances. Benefits also include better fatty acid absorption, lower infection rates, improved hepatic, renal, and immune function.
How do fatty acids in the omega-6 family influence the immune system?
Alteration of membrane structure and function, by modulation of immune function through AA metabolites, and by stimulation of inflammatory cytokines
What is Smoflipid?
A newer generation alternative ILE that is composed of a blend of soybean oil, olive oil, fish oil, and MCTs. Available in US. Contains approximately 67% less linoleic acid than soybean oil.
What is ClinOleic/Clinolipid?
A blended, alternative ILE composed of soybean and olive oil. Not commercially available in US. Contains approximately 66.2% less linoleic acid than soybean oil.
Why have commercial ILEs with high olive oil content been developed?
To reduce omega-6 fatty acid and thus the risk associated with in vivo oxidative stress and the potential for a proinflammatory environment
Describe various differences in olive-oil ILE compared to soybean oil ILE
Olive oil-based ILEs are less inhibitory of various neutrophil responses, including human neutrophil viability, phagocytic activity, inflammatory cytokine production, and oxidative burst induction. Greater immune-neutral effect
What are the benefits of MCT-LCT emulsions (50:50 w/w mixture) in PN solutions?
Providing a better oxidized energy source, improving nitrogen balance (attenuating protein catabolism in stress), and providing rapid clearance of lipid from the blood. Patients getting these emulsions have been shown to have a fatty acid profile that is closer to normal when compared with individuals who receive soybean-based ILEs
Which of the following showed improved nitrogen balance, more protection of the liver, more efficiently eliminated TGs, and a strong trend toward a shorter hospital LOS? Structured lipid, MCT-LCT PN emulsion (structured lipid group), or a physically mixed MCT-LCT PN emulsion (MCT/LCT group)?
Structured lipid group
What are the most common phytosterols and what are they?
Campesterol, sitosterol, and stigmasterol. They are plant analogues of cholesterol and are found in all currently available plant-based ILE formulations. May interfere with bile acid homeostasis
What is the hypothesis that data is consistent with regarding phytosterols in plant-based ILE formulations?
High phytosterol exposure is associated with PNALD and, reduction of soybean-based ILE and/or use of fish oil that does not contain any phytosterols can reduced the incidence of PNALD
What are the nutritionally essential amino acids?
Phenylalanine, isoleucine, leucine, lysine, methionine, threonine, tyrptophan, valine, and histidine
Describe the main functions of proteins and amino acids
- Growth, maintenance, and movement: proteins form integral parts of most body structures (skin, tendons, membranes, muscles, organs, bones). Support growth and repair of body tissues
- Enzymes: facilitate chemical reactions
- Hormones: some are made of proteins, functioning as messengers and signals and regular body processes
- Immunity: antibodies, cytokines, and chemokines are proteins; regulate gene transcription and translation through mTOR signaling pathway
- Fluid and electrolyte balance: help maintain fluid volume and the composition of body fluids
- Acid-base balance: act as buffers
- Transportation and storage: transport substances (lipids, vitamins, minerals, and oxygen); some store a specific micronutrient
What are the 4 levels of protein structure?
Primary structure, secondary structure, tertiary structure, quaternary structure
Name some examples of transport proteins
Hemoglobin (carries oxygen from lungs to the cells)
Lipoprotein (transports lipids around the body)
Retinol-binding protein (transports retinol from liver to target tissues)
Albumin
Prealbumin
What are the secretory sites, main target sites, and functions of Gastrin?
Secreted in pyloric antrum, duodenum, and pancreas
Target site is parietal cell
Acid secretion, gastric contraction
What are the secretory sites, main target sites, and functions of Secretin?
Secreted in duodenum
Main target site is pancreas
Water and bicarbonate secretion
What are the secretory sites, main target sites, and functions of Cholecystokinin?
Secreted in duodenum and jejunum
Main target sites are pancreas and gallbladder
Pancreatic enzyme secretion, gall bladder contraction
What are the secretory sites, main target sites, and functions of Gastric inhibitory peptide?
Secreted in duodenum and jejunum
Main target site is pancreas
Insulin secretion
What are the secretory sites, main target sites, and functions of Glucagon-like peptide-1?
Secreted in small intestine (L cell)
Main target site is pancreas
Insulin secretion
What are the secretory sites, main target sites, and functions of Glucagon-like peptide-2?
Secreted in small intestine (L cell)
Main target site is small intestine
Intestinal growth (crypt cell)
What are the secretory sites, main target sites, and functions of Peptide YY?
Secreted in small intestine (L cell)
Main target site is brain stem
Slowing the gastric emptying, reducing appetite
What are the secretory sites, main target sites, and functions of Somatostatin?
Secreted in pyloric antrum, hypothalamus
Main target sites are GI tract, pituitary gland
Suppressing the release of GI hormones
What are endogenous sources from which protein enters the GI tract?
Desquamated mucosal cells, digestive enzymes, other glycoproteins such as mucus
Which amino acids are the most rapidly absorbed?
Methionine, leucine, isoleucine, and valine
What percent of dietary protein is absorbed as dipeptides and tripeptides? What percent is absorbed as free amino acids?
67% and 33%
What are the limitations of of free amino acid formulas in the clinical setting?
Higher osmolality, less palatable, cost more. Elemental formulas vs polymeric did not show and advantage with the former for patients with Crohn’s disease
What factors affect the accuracy of nitrogen balance measurement?
Renal dysfunction, errors in estimating intake, or incomplete collection of urine, stool, fistula, or ostomy losses may affect balance results
What is the formula for calculating nitrogen balance (NB)?
NB = Nitrogen Intake - Nitrogen Output
What is the formula for calculating Nitrogen Output (g/day)?
Nitrogen Output (g/day) = [Urinary Urea Nitrogen (mg/100 ml) x Urinary Volume (L/d)/100] + 20% of Urinary Urea Losses + 2 gm
What are the best ways to evaluate protein adequacy after traumatic injury?
Nitrogen Balance; made easier when the sole nutrition source is PN or EN. Clinical guidelines help define protein requirements in critical illness, but it is often necessary to adjust protein goals depending on the clinical condition of the patient (eg, worsening renal function where protein may need to be decreased).
Describe the characteristics of arteriovenous amino acid differences across organs as a measure of protein metabolism
Invasive method
A tracer amino acid should be infused
Samples of blood are obtained from both the arterial and venous catheter
The measurements are made across muscle beds
Describe the characteristics of tracer methodology as a measurement of protein metabolism
Constant infusion method used in human studies
No requirement for a steady state
Ideal for measuring acute changes in patients
Important research tool
Describe the characteristics of urinary creatinine excreted over 24 hours as a measurement of protein metabolism
Indirect measurement of muscle mass
Has high variation
Describe the characteristics of urinary 3-methyl histidine excretion as a measurement of protein metabolism
Can be used as a measure of muscle degradation
Compromised accuracy with organ dysfunction
What functions are amino acids used for within the intestinal cell?
Synthesis of nucleic acids, glutathione, apoproteins as components of lipoproteins, or other nitrogen-containing compounds
Secretory protein synthesis
Act as an important energy source to the GI tract
Name the gluconeogenic amino acids
Alanine, glycine, cysteine, serine, threonine, asparagine, arginine, aspartic acid, histidine, glutamic acid, glutamine, isoleucine, methionine, proline, valine, and phenylalanine
In critically ill patients, hepatic glucose production ___ which can contribute to what condition?
Increases; hyperglycemia
What is the key role of alanine and glutamine in muscle BCAA metabolism?
They participate in the process to remove nitrogen wastes that are produced during BCAA oxidation
Which amino acid is the only one that undergoes a complete oxidation pathway in muscle (via the formation of acetyl coA)?
Leucine
Describe the role of the liver in regards to protein
Regulates the flow of dietary amino acids and other nitrogenous compounds derived from tissue degradation
Synthesizes plasma proteins
Metabolism of toxic nitrogenous wastes that have accumulated from exogenous protein intake or from protein breakdown during catabolic states (sepsis, trauma)
Carbon skeletons from gluconeogenic acids can be metabolized to glucose
Site of gluconeogenesis
Describe the role of the kidneys in regards to protein
Involved in interorgan exchange and synthesis of a variety of amino acids
Major site for arginine, histidine, and serine production
Conversion of phenylalanine to tyrosine and glycine to serine
Site of gluconeogenesis
Remove nitrogenous waste from the body (urea)
What is the hepatic metabolite of ammonia?
Urea
Describe the role of the brain and central nervous system in regards to protein
Amino acids are required for neurotransmitter synthesis (tyrosine used to synthesize catecholamines)
Inhibitory neurotransmitters (glycine and taurine)
Glutamine helps rid the brain of ammonia
Neuropeptides act as potent neurotransmitters (mediate sensory and emotional responses
Protein is the primary substrate for which metabolic process during starvation metabolism?
Gluconeogenesis
How soon does glycogenolysis (breakdown of hepatic glycogen stores) occur after fasting? How long until stores are depleted?
2-3 hours; 24 hours
Which organs are the site of gluconeogenesis and begins how soon after a meal?
Occurs in liver and kidneys, starts within 4-6 hours after last meal
After 2 days of starvation, what does the brain switch its fuel source to?
Switches from glucose to ketone bodies
What is the PDCAAS?
Protein digestibility-corrected amino acid score
represents the relative adequacy of a protein’s most limiting amino acid
What is the PDCAAS equation?
PDCAAS (%) = [mg of limiting amino acid in 1 g of test protein)/(mg of same amino acid in 1 g of reference protein)] x fecal true digestibility percentage
What would a PDCAAS of 100% mean?
That 100% of the amino acids of a protein after digestion can be used for protein synthesis, or that the protein contains all essential amino acids in adequate proportions
The nitrogen content of proteins varies from __% to __%, and nitrogen conversion factors range from __ to __
13-19%
5.26-7.69
How is the protein content for enteral and parenteral formulations determined?
Amino acid analysis; the protein content can be calculated from its amino acid concentrations
The total amount of protein provided from an IV amino acid mixture is about __% less than what would be assumed. Why?
17%
When a peptide bond is made, a molecule of water is released; thus, the weight of a peptide bond is 18 mass units less than its molecular weight
Example: to provide 1.0-1.5 gm of protein per kg of body weight via PN, how many gm of a mixed amino acid solution needs to be administered?
1.2-1.8 gm
Formula for converting nitrogen to protein
Protein = Nitrogen x 6.25
Why is there negative nitrogen balance after minor elective surgery?
Due to a decrease in protein synthesis
Why would there be a negative nitrogen balance with severe sepsis and injury?
Both protein synthesis and catabolism are elevated and feeding further increases turnover
What are the risks of feeding too much protein in critical illness?
Prerenal azotemia (with excess protein increasing the burden to the kidneys to work to excrete excess urea nitrogen). Excess protein feeding over long term can result in kidney stones and increased risk for osteoporosis
Why might metabolic rate and protein requirements for an underweight individual be higher per kg of body weight?
The more metabolically active central protein compartments (liver, heart, lungs, brain) make up a greater proportion of the total body weight; and there is a loss of both fat and muscle
What is the most abundant amino acid in the body?
Glutamine - accounts for more than 50% of the intracellular free amino acid pool in the muscle
Which amino acids serve as the body’s primary nitrogen shuttle between muscle and visceral organs?
Glutamine and alanine
Choline can be manufactured in the liver from ___
Methionine
Examples of conditionally essential amino acids under certain clinical conditions
Tyrosine, cysteine, glutamine, histidine, taurine
Amino acids with pharmacological potential
Arginine, carnitine, choline, creatine, beta-hydroxy methylbutyrate (HMB - a metabolite of leucine)
populations at risk for vitamin D deficiency
fat malabsorption, pancreatic insufficiency, decreased bile acid secretion, decreased intestinal surface area
the first part of the body to show micronutrient deficiencies
oral cavity
the first sign/symptom to detect a micronutrient deficiency
serum labs
B12 and Copper deficiency are identical, the distinguishing factor is
B12 is macrocytic and Copper is hypochromic
Non-B complex vitamins (water soluble)
B vitamins, ascorbic acid, choline
micronutrients absorbed primarily in the stomach
Intrinsic factor, alcohol, copper, molybednum
micronutrients primarily absorbed in the duodenum
iron, selenium, calcium, phosphorous, magnesium, copper, thiamine, riboflavin, niacin, folate, A,D,E,K
micronutrients primarily absorbed in the jejunum
pantothenate, vitamin B6, zinc, chromium, manganese, , thiamine, riboflavin, vitamin C, iron, magnesium, ADEK, calcium, phosphorous
micronutrients are primarily absorbed in the ileum
B12, bile salts/acids, magnesium, vitamin C, D and K
micronutrients absorbed in the large intestine
vitamin K and biotin
major micronutrients deficient in roux-en-y gastric bypass
iron, calcium, intrinsic factor, b12, copper, fluoride, vitamin D, bile salts and thiamine
most likely micronutrient deficiency with an ileal resection <100cm of terminal ileum left over
B12, sodium, bile salts/acids limiting fat absorption, limited fat soluble vitamins
micronutrient losses associated with loss of terminal ileum
B12, Bile salts, fat malabsorption, fat soluble vitamin malabsorption, decreased essential fatty acid absorption, gastric hypersecretion and SIBO B12 deficiency
if the colon is intact, bacteria can produce _____ ,____,____, and ___in the setting of a lost ileum
thiamine, riboflavin, pantothenic acid, vitamin K
is there any evidence to support vitamin A supplementation in wounds
No
deficiency of vitamin ___ can delay wound healing as scar tissue wouldn’t be able to form from collagen
vitamin C
role of vitamin E for wound healing
an antioxidant used in collagen synthesis
is vitamin E beneficial in wound healing
YES
Name the fat-soluble and water-soluble vitamins
Fat-soluble: vitamins A, D, E, and K
Water-soluble: all B vitamins, C, and choline
3 forms of Vitamin A?
Retinol, retinaldehyde (retinal), and retinoic acid
Typical form that vitamin A is ingested as?
Retinyl ester
Primary storage sites of vitamin A
Liver is primary site. Also stored in adipose tissue, kidneys, bone marrow, lungs, eyes
Role of vitamin A in wound healing?
As retinoic acid, it is needed for epithelial cell growth. Vitamin A increases the number of macrophages and monocytes in the wound during the inflammatory phase, stimulates epithelialization, increases collagen deposition by fibroblasts. Can also reverse the inhibitory effects of corticosteroids on wound healing
1 mcg of retinol is equivalent to the activity of __ mcg beta-carotene from food?
1 mcg retinol = 12 mcg beta-carotene
RAE (retinoic acid equivalent) is equal to what amount of each of the following: retinol, IU retinol, mcg food-based beta-carotene, mcg alpha-carotene, mcg beta-cryptoxanthin
1 mcg retinol
3.33 IU retinol
12 mcg food-based beta-carotene
24 mcg alpha-carotene
24 mcg beta-cryptoxanthin
How does vitamin D absorption occur?
In tandem with fat and bile salts via passive diffusion into the intestinal cell where it is packaged as chylomicrons for entrance into the lymphatic system and then into the blood
What is the first B vitamin deficiency that usually manifests in alcoholism?
Thiamine
What considerations should be made when a patient on warfarin therapy is receiving PN?
Scenario: 52 y/o M w/ stage IV colon cancer s/p chemo presents w/ severe nausea, vomiting, abd pain, and distention, last BM 5 days ago with no intake other than sips of fluids. Pt is found on CT to have an ileus and also DVT of LLE. NG placed to suction. Unable to tolerate oral feedings after 48 hours of admission so PN is started. Advanced to liquid diet and transitioned to warfarin therapy with a target INR of 2-3. During warfarin therapy INR remains subtherapeutic despite frequent increases in warfarin dose until it reaches abnormally high levels
Nutrition support clinician should assess the vitamin K intake from PN sources and its impact on warfarin dosage. PN is adjusted to decrease vitamin K to achieve therapeutic INR at a stable warfarin dose. If possible, switch patient to a multivitamin product that does not contain vitamin K, such as MVI-12 (Hospira). If lipid emulsion also provides a high dose of vitamin K, it may also be adjusted
Vitamin K content of parenteral multivitamin Infuvite? Range of vitamin K content in lipid emulsions depending on the fat source?
150 mcg vitamin K per unit dose (10 mL)
0-1000 mcg vitamin K per liter in lipid emulsions
What is an extra challenge with the provision of nutrition support to patients receiving warfarin therapy?
The variable vitamin K content in lipid emulsions along with the periodic nature of their administration (lipids given 3 times/week rather than daily)
Describe the vitamin K content of Propofol?
Propofol is 10% soybean oil. Soybean oil has approximately 1.7 mcg vitamin K per mL
How does thiamin deficiency affect nutrient metabolism?
Thiamin is necessary for the conversion of pyruvate to acetyl-CoA, a major step in the transformation of glucose to adenosine triphosphate. In the absence of thiamin, energy metabolism is impaired. As pyruvate builds up, it is driven toward lactic acid fermentation, which causes the spike in lactate and contributes to metabolic acidosis. Thiamin is necessary for the Krebs cycle enzyme alpha-ketoglutarate dehydrogenase. Together, these conditions decrease the acetyl-CoA entering the Krebs cycle from carb metabolism and limit the energy substrates produced in the Krebs cycle from fatty acid-derived acetyl-CoA
Patient scenario: Patient presents with SOB, restlessness, mild confusion. Also with severe edema in lower extremities and abdominal ascites 2/2 alcoholic liver cirrhosis. Oral intake has been inadequate for the past month due to binge drinking. Started on furosemide 40 mg. Day 2 restlessness progresses to combative behavior, increased confusion, nystagmus, leg tremor. ABG indicative of metabolic acidosis which is unresponsive to treatment. Serum Mg is 1.5, slightly below normal. What is the appropriate intervention?
Wernicke encephalopathy 2/2 thiamin deficiency is suspected. Furosemide is discontinued and replaced with oral spironolactone. Furosemide promotes urinary thiamin wasting. A multivitamin is administered along with thiamin (200mg 3x daily) for 5 days. Initial dose is given with- 1gm Mg sulfate. Confusion and agitation, as well as metabolic lactic acidosis, resolve within 6 hours of treatment. Patient sent home on oral thiamin supplement of 100mg 3x/day. Dose decreased to 100mg/day in 2 weeks
Describe the mechanisms through which severe alcoholism causes thiamin deficiency
- People with alcoholism often replace nutrient-dense energy sources with energy from alcohol intake, which can lead to malnutrition
- Ethanol inhibits intestinal thiamin absorption
- The active for of thiamin, thiamin pyrophosphate, is synthesized in the liver, making liver cirrhosis a possible contributing factor in thiamin deficiency
Thiamin deficit occurs within how many days of inadequate intake?
14-20 days
What nutrient is necessary for the conversion of thiamin to its active form, thiamin diphosphate?
Magnesium. A Mg deficiency effectively renders thiamin unusable
What is the suggested thiamin replacement for suspected Wernicke encephalopathy or Wernicke-Korsakoff syndrome (from a recent compilation of evidence, however recommendations vary widely)?
For 3-5 days: 100-200 mg IV or intramuscular thiamin 3x/day before high carb meals
For the next 1-2 weeks: 100 mg oral thiamin 3x/day
Then 100 mg oral thiamin once daily thereafter
What is the recommended treatment for confirmed Wernicke encephalopathy or Wernicke-Korsakoff syndrome?
200-500 mg IV or intramuscular thiamin 3x/day for 5-7 days
100 mg oral thiamin 3x/day for the next 1-2 weeks
Then 100 mg oral thiamin once daily thereafter
Which essential amino acid can synthesize the coenzyme nicotinamide adenine dinucleotide (NAD)?
Tryptophan. 60 mg tryptophan produces 1 mg niacin
Nutrients of concern when a tuberculosis patient is being treated with Isoniazid?
Niacin (B3), Vitamin B6 (pyridoxine)
Besides inadequate iron intake, what other mineral deficiencies or excesses may create hematological indices consistent with iron deficiency anemia and why?
Copper deficiency interferes with iron absorption and thus effectively creates copper deficiency anemia (iron deficiency anemia in patients with iron replete status). Zinc toxicity creates a copper deficiency, initiating the same mechanisms. Chromium toxicity can contribute to iron deficiency anemia due to its receptor site competition with iron
Which cells in the GI tract secrete more than 30 GI hormone peptides?
Neuroendocrine cells
What are the major inputs influencing appetite regulation?
Short term signals related to meal ingestion that are transmitted by the “gut-brain” axis
Signals associated with energy stores that are mediated by leptin
Signals deriving from lean body mass
Circadian rhythm
What is the major orexigenic (appetite stimulating) gut hormone?
Ghrelin
Name anorexigenic (appetite suppressing) gut hormones
Glucagon-like peptide-1 and -2 (GLP-1, GLP-2)
Oxyntomodulin (OXM)
Peptide tyrosine-tyrosine (PYY)
Pancreatic polypeptide (PP)
Cholecystokinin (CCK)
How are gut- and fat-derived hormones (ghrelin, leptin, insulin, and PYY) involved in feedback regulation of feeding?
Through signals affecting hunger, satiety, and energy needs
How does ghrelin increase food intake?
By stimulating the ARC of the hypothalamus
Where in the brain are neural and hormonal signals that influence food intake located?
The arcuate nucleus (ARC) of the hypothalamus and the brainstem
Name the site of secretion, stimulating factors, mechanism of action, and effect of GLP-1 (glucagon-like peptide-1)
Distal gut
Stimulated by food intake proportional to energy intake
Works by binding GLP-1 receptors in pancreatic islet cells, heart, lungs, and brain (ARC and PVC)
Reduces appetite and energy intake; delays gastric emptying; enhances postprandial insulin release
Name the site of secretion, stimulating factors, mechanism of action, and effect of OXM (oxyntomodulin)
L cells of the distal gut
Stimulated by food intake
Works as agonist at glucagon receptor; has undefined neural effects
Reduces food intake; increases energy expenditure
Name the site of secretion, stimulating factors, mechanism of action, and effect of PYY (peptide-tyrosine-tyrosine)
L cells of the distal gut
Stimulated by food intake (released in proportion to energy, fat, and protein intake)
Mechanism of action: Y receptors found throughout the CNS and on vagal afferents, NPY (neuropeptide Y) inhibition, POMC (proopiomelanocortin) activation, associated with increased activity of OFC (orbitofrontal cortex)
Reduces food intake
Name the site of secretion, stimulating factors, mechanism of action, and effect of PP (pancreatic polypeptide)
Pancreatic polypeptide cells of the islets of Langerhans in the pancreas
Stimulated by food intake and vagal stimulation
Enters CNS via diffusion in the brain stem and ARC
Reduces food intake
Name the site of secretion, stimulating factors, mechanism of action, and effect of CCK (cholecystokinin)
L cells of the gut, nerves in distal ileum and colon, neurons in the brain
Stimulated by dietary protein and fat, gastric acid
Reduces hypothalamic NPY (neuropeptide Y)
Inhibits gastric emptying and reduces food intake
Name the site of secretion, stimulating factors, mechanism of action, and effect of Leptin
Large amounts from the gastric mucosa; white adipose tissue
Food deprivation is associated with low levels
Low levels influence ARC; possibly decreases gene expression of NPY and increases activity of POMC-secreting neurons
Low levels increase energy intake and decrease energy expenditure
Name the site of secretion, stimulating factors, mechanism of action, and effect of Ghrelin
Stomach
Food intake decreases levels; fasting increases levels
Stimulates ARC via receptors; stimulated GH secretion
Increases food intake
Describe the role of fiber (especially resistant starch R2) on the feeding response
It has satiety value with associated decreases in food intake
True or false: stomach size can influence the amount of food eaten
True. Its size is related to the amount of food habitually eaten.
How is aging associated with decreased appetite and food intake
Likely because of decreased basal hunger rather than increased meal satiety
Name some adverse effects that have been associated with megestrol
Nausea, vomiting, gas, diarrhea
GI muscle fibers are depolarized (contraction of the muscle) in response to?
Stretching of the muscle fiber
Acetylcholine released by parasympathetic neurons
Gut hormones
Inhibition of GI muscle contraction is associated with a hyperpolarized state which is caused by?
Norepinephrine or epinephrine
Sympathetic nerves that secrete norepinephrine
How is the enteric nervous system connected to the central nervous system?
By parasympathetic fibers (stimulates motility) and sympathetic fibers (modulates activity of ENS with inhibitory signals)
Factors that regulate gastric emptying
Volume of food
Gastrin
Enteric gastric nervous reflexes from the duodenum
Ghrelin
Hormonal feedback from the duodenum
What are the neurotransmitters of the ENS?
Acetylcholine
Norepinephrine and serotonin
y-aminobutyrate
Adenosine triphosphate (ATP)
Nitric oxide (NO) and carbon monoxide (CO)
Dopamine
CCK
Substance P
Vasoactive intestinal peptide (VIP)
Somatostatin
Leu-enkephalin
Met-enkaphalin
What are some sensory stimuli in the ENS that are involved in the neural control of the gut?
Irritation of the mucosa, excessive distention, or chemical stimuli
Describe the stimuli for secretion, site of secretion and action of gastrin for GI motility
Stimuli are protein, GI distention, gastric-releasing peptide
Secreted by G cells of the antrum, duodenum, and jejunum
Stimulates gastric acid secretion and mucosal growth; promotes gastric emptying
Describe the stimuli for secretion, site of secretion, and action of cholecystokinin for GI motility
Stimuli are protein, fat, and acid
Secreted by I cells of the duodenum, jejunum, and ileum
Stimulates pancreatic enzyme secretion, gallbladder contraction, and growth of exocrine pancreas; inhibits gastric emptying
Describe the stimuli for secretion, site of secretion, and action of secretin for GI motility
Stimulus is acid
Secreted by S cells of the duodenum, jejunum, and ileum
Stimulates pepsin, pancreatic and biliary bicarbonate secretion, and growth of exocrine pancreas; inhibits gastric emptying and gastric acid secretion
Describe the stimuli for secretion, site of secretion, and action of gastric inhibitory peptide (GIP) for GI motility
Stimuli are protein, fat, carbohydrate
Secreted by K cells of the duodenum and jejunum
Stimulates insulin release and secretion; inhibits gastric acid secretion and emptying
Describe the stimuli for secretion, site of secretion, and action of motilin for GI motility
Stimuli are fat, acid, gastric distention, bile acids, serotonin, and low pH in duodenum
Secreted by M cells of the duodenum and jejunum, stomach, colon
Stimulates gastric motility and intestinal motility
Describe the stimuli for secretion, site of secretion, and action of vasoactive intestinal peptide (VIP) for GI motility
Stimulus is GI distention
Secreted by nerves of the GI tract
Stimulates secretion of electrolytes and water secretion; inhibits gastric acid
Describe the stimuli for secretion, site of secretion, and action of somatostatin for GI motility
Stimulus is acid
Secreted by pancreas, GI mucosa, hypothalamus
Inhibits secretion of gastrin, VIP, GIP, secretin, motilin, exocrine pancreatic secretion, gallbladder contraction, gastric acid secretion, and gastric motility
Describe the stimuli for secretion, site of secretion, and action of serotonin (5-HT) for GI motility
Stimuli are luminal contents including glucose and SCFAs, GI distention
Secreted by nerve fibers of the enteric nervous system
Increases intestinal motility
Describe the stimuli for secretion, site of secretion, and action of peptide-tyrosine-tyrosine (PYY) for GI motility
Stimulus is fat
Secreted by jejunum
Inhibits gastric acid secretion and gastric motility
What motor functions of the stomach contribute to digestion?
Storing food, mixing food with gastric secretions, and emptying the semifluid mixture (chyme) into the duodenum
What factors decrease gastric tone?
Duodenal distention, colonic distention, ileal perfusion with glucose
The inhibitory reflexes of the duodenum are stimulated by what 5 factors?
- duodenal distention
- irritation of the duodenal mucosa
- pH less than 3.5 or 4.0
- high osmolality
- the presence of breakdown products of protein and fat digestion
Which macronutrient is the strongest stimulus for hormones of the duodenum and jejunum?
Dietary fat
The tone of which portions of the stomach influence liquid and solid emptying?
Proximal stomach influences liquid emptying
Distal stomach is involved in solid emptying
What is the average half-emptying time of water or isotonic saline?
12 minutes
Example: if one drinks 300 ml of water, 150 ml will enter the duodenum in about 12 minutes
What factors regulate liquid emptying?
Duodenal osmoreceptors, secretin, and VIP
What is the half-emptying time of solids?
45-110 minutes
Intragastric pressure ____ in response to the swallowing reflex and in response to gastric distention by the presence of food
Falls
What is the volume that a relaxed stomach can hold?
0.8 to 1.5 L
What factors influence the rate of gastric emptying time of solids?
Meal particle size, energy content, and fat content
When the swallowing mechanism is bypassed, such as in NG feeding, the rate of gastric emptying is ______.
Faster
Why would gastric emptying time decrease if feeding tubes are placed in the jejunum, bypassing the duodenum?
The duodenal mucosa possesses sensory receptors that are associated with neurohormonal reflexes that influence gastric emptying time
What factors determine the amount of chyme that enters the intestine from the stomach?
Duodenal distention, acidity, osmolar changes, and the presence of products of carbohydrate, protein, and fat digestion
When are segmentation contractions (mixing contractions) of the small intestine elicited?
When the small intestine is distended by chyme
What is the average time it takes for chyme to travel from the pylorus to the ileocecal valve?
3-5 hours. The rate of mixing contractions is 2-3 per minute or maximally 12 per minute. Propulsive movements of the small intestine (peristalsis) move in the direction of the anus at a rate of 0.5-2.0 cm/second.
When is neural control partly initiated during intestinal peristalsis?
When chyme stretches the intestinal wall
What are the stimulatory hormones of intestinal peristalsis?
Gastrin, CCK, insulin, motilin, and serotonin
What is the volume of chyme that empties into the cecum?
1500-2000 ml/day
What is the purpose of the ileocecal valve?
To prevent backflow of fecal content into the small intestine
How long does it take for chyme to move from the ileocecal valve through the colon?
8-15 hours
On average, after abdominal surgery, the small intestine regains peristalsis within ____ hours (or sooner), and motility of the stomach and colon returns between ____ and ____ hours
24, 48, 72
In a previously well-nourished patient, parenteral nutrition should only be considered after how many days of NPO?
7 days. PN has been associated with higher infection morbidity in previously well-nourished patients compared with standard care
Aside from abdominal surgery, what other conditions/situations can cause ileus?
Infection, inflammation, electrolyte imbalance, the use of certain drugs such as sedatives, opioid analgesics, a2-adrenergic receptor agonists, catecholamine vasopressors
Name potential etiologies or contributing factors of ileus?
Opiate use, sympathetic hyperactivity, altered spinal-intestinal neural reflexes, changes in hormone expression and secretion, hypomagnesemia, hypokalemia, and local and systemic inflammation
What is chronic intestinal pseudo-obstruction (CIP)?
A motility disorder of peristalsis that most often affects the small bowel but can occur at any point in the GI tract
Name the secondary causes of CIP
Collagen vascular and endocrine diseases, neurological diseases, medication-related effects
Describe the treatment plan for CIP
Palliation of symptoms including nausea and vomiting with antiemetics and/or prokinetics, provision of IV hydration or PN, nocturnal cyclic EN when possible, and, when necessary, withholding of oral intake of food
What is the preferred mode of nutrition for CIP?
Oral
Describe the MNT for CIP patients who can consume an oral diet
Recommend small, frequent meals low in fat and fiber, with an emphasis on liquid forms of energy and protein. Daily multivitamin and mineral supplement is recommended, and if the patient has small intestinal bacterial overgrowth (SIBO), emphasis should be placed on fat-soluble and B12 vitamins.
List serious consequences of diarrhea
Severe fluid and electrolyte abnormalities; fluid loss, dehydration, hypovolemia; hypovolemic shock and cardiovascular collapse; increased risk of pressure ulcers, compromised nutrition status, increase hospital LOS
What percent of cases of antibiotic-associated diarrhea (AAD) is from C. difficile infection?
20%
What is the standard recipe for oral rehydration solution published by the World Health Organization?
2.6 gm NaCl, 13.5 gm anhydrous glucose, 1.5 gm potassium chloride, 2.9 gm trisodium citrate, and 1 L water
What MNT should be offered to a patient who has reobstruction of the small intestine after surgery (lysis of adhesions) for small bowel obstruction?
If the patient has a normal nutrition status on admission, the best nutrition intervention is no initial intervention. Would keep patient NPO on bowel rest and evaluate for PN on hospital day 7
What enteral MNT would you offer to a patient with severe diarrhea related to C.diff pseudomembranous colitis (PMC)?
Evidence-based diet recommendations for PMC diarrhea have not been established, however the goal is to initiate nutrition through the GI tract as early as possible to limit gut mucosa atrophy. Would keep patient NPO until diarrhea improves of antibiotic therapy, then initiate on caffeine-free clear liquids, and then advance to low-lactose, low-fat, low-fiber diet. Supplemental fiber use in C.diff diarrhea is not supported by ASPEN. IV fluids if oral intake does not keep up with losses. PN should not be offered unless patient presents severely malnourished.
How do SCFAs help control diarrhea?
By stimulating the uptake of water and electrolytes by colonocytes
Name some causes of gastroparesis
Diabetes mellitus (at least 25% of cases), complications of surgery, renal disease, collagen disease, drugs, malignancy, hypothyroidism, and possible idiopathic reasons
What surgical intervention can be offered for a patient who fails medical treatment for gastroparesis?
A near-total gastrectomy and Roux-en-Y gastrojejunostomy.
What are the dietary treatments for gastroparesis?
Small, frequent meals, drinking fluids with meals, limiting dietary fat and fiber, maintaining good glucose control, and, when necessary, feeding past the pylorus
What nutrition intervention is recommended for a patient with gastroparesis who has failed to respond to dietary intervention?
Jejunostomy-tube placement for long-term intestinal feedings and oral diet of small amounts of low-fat, low-fiber foods with liquids as tolerated (to address the psychosocial need to eat). If patient is receiving nighttime cyclic feedings, may also need to change to a longer-acting insulin to control glucose levels during nighttime feeding. Jejunal feedings bypass the stomach and obviate the potential of formula intolerance associated with delayed gastric emptying.
Name conditions associated with constipation
Diabetes mellitus, hypothyroidism, hypercalcemia, dehydration, neurologic disorders, anorectal disease, and collagen vascular/muscular diseases
What are the first-line medication treatments for constipation when nonpharmacological approaches fail? Second-line?
First-line: Hydrophilic colloids (psyllium, bran methylcellulose, polycarbophil), stool softeners, osmotic laxatives (polyethylene glycol, lactulose, sorbitol, and magnesium salts).
Second-line: Stimulants (senna/docusate, bisacodyl/docusate, or casanthranol/docusate) and lubricants (mineral oil).
What is the disadvantage of using mineral oil for constipation?
It binds fat-soluble vitamins and, if aspiration occurs, could cause a lipoid pneumonia.
What is dumping syndrome?
A group of symptoms that develop after gastric surgery and are related to increased gastric emptying following vagotomy and bypass or destruction of the pylorus. Can also occur with too rapid infusion of EN through a small-bore feeding tube. It is accompanied by both GI symptoms and vasomotor symptoms.
What are the GI and vasomotor symptoms of dumping syndrome?
GI symptoms: feeling of fullness after eating, crampy abdominal pain, nausea, vomiting, and explosive diarrhea
Vasomotor symptoms: diaphoresis, weakness, dizziness, flushing, and palpitations
What are the time frames for early vs late dumping?
Early: within 30-60 minutes of eating
Late: occurs 2-3 hours after eating and is limited to vasomotor symptoms
What is the cause of the GI and vasomotor symptoms of dumping syndrome?
GI: related to the rapid emptying of hyperosmolar chyme into the small intestine from the stomach, eliciting an osmotic diuresis into the intestinal lumen and subsequent distention
Vasomotor: rapid delivery of glucose to the upper small intestine, which results in peripheral and splanchnic vasodilation. This rapid delivery precipitates and increased serum insulin release followed by hypoglycemia and vasomotor symptoms
What is the dietary treatment for dumping syndrome?
Involves slow introduction of solid food, elimination of simple sugars, frequent small meals, and no liquids with meals. Patients are advised to lie down after eating and consider adding functional fibers to delay gastric emptying. The initial post-op period should not include simple sugars. Dairy products should be restricted initially because temporary lactose intolerance may occur. Liquid multivitamin/mineral supplements and vitamin B12 injections may be warranted in patients who have undergone a gastric resection.
What are the 2 primary functions of secretions in the GI tract?
To supply digestive enzymes and to supply lubricating mucus
What populations are at risk for xerostomia?
Obese patients, older adults, patient’s with Sjogren’s syndrome, those undergoing radiotherapy or chemotherapy for cancer, those with hormone disorders and infections
What are some consequences of hyposalivation?
Alterations in taste perception, chewing and swallowing problems, intolerance of spicy foods, can encourage dietary choices that compromise nutrition status and increase the risk for dental plaque and periodontal disease
How does hyposalivation occur with obesity?
Via increased leptin and decreased ghrelin
What are the contents of saliva?
Mucin (for lubrication), ptyalin (alpha-amylase; enzyme for starch digestion), immunoglobulin A (IgA), lysozyme (for protection against oral bacteria), components that play a role in innate immunity
How much saliva do humans secrete each day?
Approximately 1000-1500 ml/day
Where do gastric secretions derive from?
Mucus-secreting cells, oxyntic glands (gastric glands), and pyloric glands
What 3 cells make up oxyntic glands?
Mucus-producing cells, peptic (chief) cells, and parietal cells
Peptic cells secrete ___ and ___; parietal cells secrete ___ and ___.
Pepsinogen and gastric lipase
Hydrogen chloride (HCl) and intrinsic factor
What is the pH of the gastric acid?
Approximately 0.8
What is a possible consequence of the destruction of parietal cells, such as with chronic gastritis?
Achlorhydria (the absence of acid) develops in addition to pernicious anemia and vitamin B12 deficiency caused by loss of intrinsic factor. Intrinsic factor is required for the absorption of vitamin B12 and is secreted by the same cells that secrete HCl
What are the biochemical stimulants for acid secretion?
Gastrin, histamine via H2 receptors, and acetylcholine released by parasympathetic stimulation
Gastrin is secreted in response to the presence of ___
Luminal oligopeptides (peptide products of protein digestion), gastric distention, and GRP (bombesin)
The presence of carbohydrate, protein, or fat in the duodenum ____ gastric acid and pepsin secretion as well as gastric motility
Inhibits
Caffeine and alcohol ____ gastrin and acid production
Stimulate
Peptic ulcers develop when ____ is compromised
The gastric lining’s protective barrier against irritation and autodigestion
What is the treatment for peptic ulcers?
Suppression of gastric acid production, ie. Proton-pump inhibitors (exert their effects on acid suppression by interfering with hydrogen potassium ATP activity), H2-receptor antagonist drugs (block histamine stimulation of acid production)
What are the 3 phases in which gastric juice is secreted?
- Cephalic phase
- Gastric phase
- Intestinal phase
Describe the cephalic phase of gastric juice secretion
Acid is secreted via vagal stimulation in response to the sight, smell, and/or taste of food. Vagus nerve releases acetylcholine (stimulates ECL cells and parietal cells). Accounts for 30% of the volume of acid secretion.
Describe the gastric phase of gastric juice secretion
Begins when food arrives in the stomach. Amino acids and peptides stimulate the G cells in the antrum to produce gastrin (enters the general circulation and stimulates parietal cells as an endocrine hormone). Gastric distention also leads to acid secretion via a reflex involving the vagus nerve. Accounts for 60% of the volume of acid secretion.
Describe the intestinal phase of gastric juice secretion
Food in the duodenum continues to stimulate small amounts of gastric secretions (likely related to the small amount of gastrin that is secreted by the duodenal mucosa). Accounts for approximately 10% of gastric acid secretion.
Describe the multiple ways in which gastric secretions are inhibited by signals from the intestines
Food in the small intestine stimulate gastrin release and initiates a reverse enterogastric reflex that inhibits gastric secretions. The presence of acid, fat, products of protein digestion, hyper- or hypotonic fluids, or irritants in the proximal small bowel stimulate the secretions of gastric secretion-inhibiting hormones (secretin, GIP, VIP, somatostatin). The presence of carb, protein, or fat in the duodenum inhibits gastric acid and pepsin secretion and gastric motility.
What are the components of bile?
Water, bile salts, bile pigments, cholesterol, lecithin, fatty acids, and electrolytes
What are the two principal bile acids?
Cholic acid and chenodeoxycholic acid
What are the secondary bile acids that are converted by colonic bacteria?
Cholic acid converts to deoxycholic acid
Chenodeoxycholic acid converts to lithocholic acid
What are the bile pigments?
Bilirubin and biliverdin
Describe jaundice and how it can be detected
Jaundice occurs in pathological conditions when bilirubin accumulates in the blood, skin, sclera, and mucous membranes. It imparts a yellow color and can be detected when total plasma bilirubin exceeds 2 mg/dL
Bile production is stimulated by ___ and ___
The vagus nerve and secretin
What is the sphincter of Oddi?
The exit of the common bile duct into the duodenum. It remains closed between meals, directing bile to the gallbladder. It relaxes (opens) after a meal (especially if it is high in fat) when the gallbladder contracts. Relaxation of the sphincter is mediated by the action of CCK
How much bile is secreted per day?
Approximately 500 mL
What is enterohepatic circulation?
Reabsorbed bile salts (90-95% of which are reabsorbed in the terminal ileum) and bile pigments are transported to the liver via the portal vein and then are reexcreted in the bile
What is the role of bile salts in the digestion of fat?
To act as emulsifiers along with phospholipids and monoglycerides
In the fasting state without any EN, gastric secretions can amount to ___ to ___ mL/day, and biliary and pancreatic secretions can be up to ____ to ____ mL/day.
500-1000 mL/day
1000-2000 mL/day
When colonic pressure increases, the ileocecal valve ____. When ileal pressure increases or when food exits the stomach, the ileocecal valve ___.
Shuts
Opens
Brunner glands secrete ___
Mucus, to protect the duodenum from gastric acid
Pancreatic secretions, intestinal secretions, and bile neutralize gastric acid to raise the pH of duodenal contents to ___
6-7
Name the pancreatic enzymes found in pancreatic juice
Carbohydrate - pancreatic amylase
Protein - pancreatic proteases (trypsin, chymotripsin, carboxypolypeptidase, proelastase, collagenase)
Fat - pancreatic lipase, cholesterol esterase, phospholipase
Why do oral rehydration solutions used to treat Na+ and water losses from diarrhea contain NaCl and glucose?
Na+ facilitates the absorption of glucose, some amino acids, and bile acids
What percent of dietary iron is absorbed under conditions of iron deficiency?
3-6%
Iron absorption is inhibited by:
Phytates in cereal, phosphates, and oxalates. These compounds for insoluble compounds with iron
Does the passage of feces continue during prolonged bowel rest when patients are restricted from consuming food?
Yes, fecal contents include material other than food residue. Feces contains bacteria (comprises 30% of the dry weight of fecal matter), inorganic material, fiber, water, sloughed off undifferentiated stem cells
How are medium-chain triglycerides absorbed?
MCTs are water soluble, they do not require the formation of micelles or the action of bile salts. MCTs are hydrolyzed and pass through enterocytes directly into the portal circulation. MCTs may be used as an energy supplement in patients who maldigest or malabsorb fat
What percent of cardiac output is delivered to the splanchnic circulation at rest?
25%
What percent of total body oxygen is consumed at rest by the splanchnic organs?
30%
During feeding, splanchnic blood flow increases __% to __% and oxygen demand in the splanchnic-supplied organs increases up to __%
40% to 60%
30%
Where does all blood in the GI tract, including the spleen and pancreas, flow to?
To the liver via the portal vein
What is the reticuloendothelial system?
A system of macrophages that clears the blood of bacteria and other particulate matter to prevent systemic infection before blood leaves the liver. In the liver, blood encounters RED cells in the lining of sinusoids (liver blood cells).
Name the arteries that supply blood to the small intestine. The stomach?
Superior and inferior mesenteric arteries (branch off the aorta) for the small intestine. Celiac artery for the stomach.
When does mucosal atrophy occur?
During starvation, stress, PN, and bowel rest
True or false: the bowel mucosa requires luminal nutrients to supply its nutrient needs
True. After 1 week of a protein-deficient diet, the microvilli shorten
What is the principal metabolic fuel for intestinal cells?
Glutamine. Its absence may directly contribute to mucosal atrophy that accompanies bowel rest.
When should EN be withheld in patients with hypoperfused gut?
When patients are being initiated on catecholamines, when catecholamine doses are increasing, or when patients require a high level of hemodynamic support including high-dose catecholamines (norepinephrine, epinephrine, dopamine) to maintain cellular perfusion.
