Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
183 Cards in this Set
- Front
- Back
|
Water soluble vitamins |
B1 (thiamin) B2 (riboflavin) Niacin B6 (pyridoxine) B12 (cobalamin) Folic acid Pantothenic acid Biotin C (ascorbic acid) 9 total |
|
|
Fat soluble vitamins |
A (retinol) D (calciferol) E (tocopherol) K |
|
|
Except for vitamin C, all water soluble enzymes have been shown to function as |
coenzymes |
|
|
Fat soluble vitamins act somewhat like |
hormones |
|
|
mineral (define) |
a metal/nonmetal used in the body in the form of ions/compounds |
|
|
Major minerals (7 total) |
calcium chlorine magnesium phosphorus potassium sodium sulfur present >5g |
|
|
Trace minerals (15 total) |
arsenic cobalt copper chromium fluorine iodine iron manganese molybdenum nickel selenium silicon tin vanadium zinc present <5g |
|
|
vitamins are organic or inorganic? |
organic |
|
|
B1 (thiamin) dietary sources |
bread, beans, nuts, milk, peas, pork, rice bran |
|
|
B1 (thiamin) functions |
coenzyme in decarboxylation reactions |
|
|
B1 (thiamin) deficiency conditions |
beriberi: nausea, severe exhaustion, paralysis |
|
|
B2 (riboflavin) dietary sources |
milk, meat, eggs, dark green vegetables, bread, beans, peas |
|
|
B2 (riboflavin) functions |
forms the coenzymes FMN and FAD, which are hydrogen transporters |
|
|
B2 (riboflavin) deficiency conditions |
Dermatitis |
|
|
Niacin dietary sources |
meat, whole grains, poultry, fish |
|
|
niacin functions |
forms the coenzyme NAD+, which is a hydride transporter |
|
|
niacin deficiency conditions |
pellagra: weak muscles, no appetite, diarrhea, dermatitis |
|
|
B6 (pyridoxine) dietary sources |
meats, whole grains, poultry, fish |
|
|
B6 (pyridoxine) functions |
coenzyme form carries amino and carboxyl groups |
|
|
B6 (pyridoxine) deficiency conditions |
dermatitis, nervous disorders |
|
|
B12 (cobalamin) dietary sources |
meat, fish, eggs, milk |
|
|
B12 (cobalamin) functions |
coenzyme in amino acid metabolism |
|
|
B12 (cobalamin) deficiency conditions |
rare except in vegetarians/people with decresed hydrochloric acid; pernicious anemia (autoimmune disorder that impairs secretion of hydrochloric acid and intrinsic factor in the stomach; ppl with this often need regular B12 shots), megaloblastic macrocytic anemia (large, fragile RBCs), nerve damage if prolonged deficiency |
|
|
folate dietary sources |
leafy green vegetables, peas, beans |
|
|
folate functions |
coenzyme in methyl group transfers |
|
|
folate deficiency conditions |
anemia |
|
|
pantothenic acid dietary sources |
all plants and animals, nuts, whole grain cereals |
|
|
pantothenic acid functions |
part of coenzyme A, acyl group carrier |
|
|
pantothenic acid deficiency conditions |
anemia |
|
|
biotin dietary sources |
found widely; egg yolk, liver, yeast, nuts |
|
|
biotin functions |
coenzyme form used in fatty acid synthesis |
|
|
biotin deficiency conditions |
dermatitis, muscle weakness |
|
|
Vitamin C (ascorbic acid) dietary sources |
citrus fruits, tomatoes, green pepper, strawberries, leafy green vegetables |
|
|
Vitamin C (ascorbic acid) functions |
synthesis of collagen for connective tissue |
|
|
Vitamin C (ascorbic acid) deficiency conditions |
scurvy; tender tissues, weak, bleeding gums, swollen joints |
|
|
Vitamin A (retinol) dietary sources |
eggs, butter, cheese, dark green and deep orange vegetables |
|
|
Vitamin A (retinol) functions |
synthesis of visual pigments |
|
|
Vitamin A (retinol) deficiency conditions |
inflamed eye membranes, night blindness, scaliness of skin |
|
|
Vitamin D (calciferol) dietary sources |
fish-liver oils, fortified milk |
|
|
Vitamin D (calciferol) functions |
regulation of calcium an phosphorus metabolism |
|
|
Vitamin D (calciferol) deficiency conditions |
rickets: malformation of the bones |
|
|
Vitamin E (tocopherol) dietary sources |
whole-grain cereals, margarine, vegetable oil |
|
|
Vitamin E (tocopherol) functions |
prevention of oxidation of vitamin A and fatty acids |
|
|
Vitamin E (tocopherol) deficiency conditions |
breakage of red blood cells |
|
|
Vitamin K dietary sources |
cabbage, potatoes, peas, leafy green vegetables |
|
|
Vitamin K functions |
synthesis of blood-clotting substances |
|
|
Vitamin K deficiency conditions |
blood-clotting disorders |
|
|
vitamin K2 name (and where is it synthesized?) |
menaquinone (synthesized in large intestine) |
|
|
Vitamin K is essential for |
vitamin K-dependent coagulation proteins(factors II, VII, IX, and X)
|
|
|
vitamin K deficiency can result in |
bleeding disorders |
|
|
who is at risk of vitamin K deficiency? |
infants up to 6 months of age. haemorrhagic disease of the newborn vitamin K deficiency bleeding (VKDB) Babies are given a vitamin K shot after birth |
|
|
Vitamin A is a |
retinoid (retinol, retinal, retinoic acid, retinyl esters) |
|
|
Vitamin A obtained in diet as |
retinol and retinyl esters |
|
|
food sources of vitamin A |
liver, eggs, fish |
|
|
beta-carotene and vitamin A link? |
bets-carotene can be converted to vitamin A in the body |
|
|
beta-carotene food sources |
leafy greens, yellow/orange veggies |
|
|
Vitamin A functions |
regulation of immune function and growth/development 2 forms act as steroid hormones, bind to receptors on nucleus and regulate gene expression by binding to DNA retinol works in the retina of the eye to convert light into a nerve impulse |
|
|
RDA for vitamin A is listed as |
retinol activity equivalents (RAE) |
|
|
What is included in RAE? |
preformed vitamin A and beta-carotene |
|
|
Vitamin A deficiency |
night blindness (inability to see in dim light) rare in developed countries |
|
|
Preformed Vitamin A toxicity |
hypervitaminosis A - liver damage, haemorrhage, death during pregnancy may cause birth defects (teratogenic) |
|
|
Beta-carotene toxicity |
carotenodermia- yellowing of skin (hypervitaminosis A is not a concern because excess beta-carotene is not converted to retinol) |
|
|
folate is the form of the vitamin in _____ folic acid is the______ |
foods; synthetic form used in supplements |
|
|
B12 absorption |
B12 in food is bound to protein, requires hydrochloric acid and a gastric protease to release B12 Then, intrinsic factor (secreted by parietal cells of stomach) must bind B12 in order to be absorbed in the ileum |
|
|
Iron- where is it in the body? |
2/3 of it are in hemoglobin some in myoglobin (a protein that helps supply oxygen to muscle cells) |
|
|
Iron in plasma must be bound to |
transferrin (carrier protein) |
|
|
Iron- forms if dietary iron and food sources |
Heme iron- derived from hemoglobin; found in meat (more easily absorbed) nonheme iron- beans, spinach, iron-enriched foods |
|
|
Iron- nonheme iron food combinations that help/hurt absorption |
help- combining with vit C Hurt- tannins in tea, phytates in legumes and whole grain |
|
|
iron absorption |
increases when stores are low, decreases when stores are high |
|
|
ferritin |
a protein that stores iron in the body. it can sequester/release iron depending on body's needs |
|
|
iron- how does spleen help iron levels |
spleen recycles the iron from old, degraded blood cells |
|
|
most common deficiency in the world |
iron (especially in women and children) |
|
|
most common toxicity in the world |
iron overdose hemochromatosis- iron overload; excessive iron accumulation in tissues |
|
|
Iron deficiency anemia characterization and testing |
small, pale RBCs containing inadequate hemoglobin blood test for hemoglobin and hematocrit (% of RBCs in blood by volume) (furthur workup can include serum transferrin saturation and serum ferritin) |
|
|
iodine sources |
seafood, plants if grown in iodine rich soil, iodized salt |
|
|
iodine uses |
required for synthesis of thyroidhormones thyroxine (T4) and triiodothyronine (T3). T4 is converted to the active form ofT3. Similar to steroid hormones, T3 canbind to intracellular receptors to regulate gene expression. Hence,thyroid hormones regulate a wide variety of processes such as glucosehomeostasis, heart rate, blood pressure, body temperature, andgrowth/development. |
|
|
Thyroidstimulating hormone (TSH)
|
secretedby the pituitary stimulates the thyroid gland in the neck to take up iodinefrom the blood for synthesis of thyroid hormones.
|
|
|
goiter |
enlarged thyroid gland in the neck caused by inadequate dietary iodine intake |
|
|
cretinism |
birth defect caused by iodine deficiency during pregnancy. mental retardation, dwarfism, deaf, mute |
|
|
calcium uses in body |
bone mineralization, muscle contraction, transmission of nerve impulses, cell signaling pathways |
|
|
calcium food sources |
dairy foods, spinach (oxalic acid in spinach binds calcium and prevents its absorption) juices and grains are often fortified with calcium |
|
|
serum calcium range and toxicity/deficiency |
~8.8-10.4 mg/dl hypocalcemia- low serum calcium, could lead to hypocalcemic tetany hypercalcemia- high serum calcium, could lead to calcification of soft tissues |
|
|
Calcium homeostasis isregulated by
|
parathyroid hormone (PTH) and Vitamin D
|
|
|
calcium homeostasis |
When serum calcium levels fall, the parathyroid gland secretesPTH. PTH stimulates: •boneresorption so that calcium isreleased from bone •renaltubules to reabsorb calcium so that less calcium is lost in urine •kidneysto synthesize and secrete 1,25(OH)2D •As described in the section on vitamin D, active vitamin D [calcitriol = 1,25(OH)2D]promotes calcium absorption in the small intestine. 1,25(OH)2D can also work with PTH to increase serum calcium by bone resorption and renal reabsorption. Both PTH and calcitriol (active vitamin D)are regulated by negative feedback, so when serum calcium levels rise, theactions listed above are reversed. |
|
|
Why do people with chronic kidney disease (CKD) have difficulty maintaining appropriate levels of calcium and phosphorus in the blood? |
Thekidneys are not able to adequately reabsorb calcium or hydroxylate vitamin D, socalcium and 1,25(OH)2D supplements are oftennecessary. In CKD patients, phosphorus(which is ubiquitous in many foods) is not adequately excreted by the kidneys,so dietary restriction of phosphorus and/or phosphate binder medications areoften needed.
|
|
|
antioxidants |
Vit E, vit C, beta-carotene, several trace minerals. counter free radical damage by preventing its formation or converting it to more stable molecules |
|
|
Free radicals |
atoms/molecules w/ 1+ unpaired electrons |
|
|
Why are free radicals dangerous? |
they are highly reactive. the unpaired electron will try to become a pair by reacting with molecules like DNA, proteins, lipids, etc. damaging these molecules. normal biological processes, like the electron transport chain, will generate free radicals |
|
|
metalloenzymes |
counter oxidative damage trace minerals (selenium, magnesium, copper, zinc) |
|
|
major storage form of energy in body |
triglycerides |
|
|
During digestion, dietary triglycerides arehydrolyzed to
|
glycerol, monoglycerides, andfree fatty acids.
|
|
|
triglycerides are resynthesized where?
|
Inside mucosal cells of the small intestine
|
|
|
chylomicrons
|
Triglycerides (along with phospholipids,cholesterol, and fat-soluble vitamins) combined with proteins
lipoprotein particles containing lipids from the diet (mostlytriglycerides) and a small amount of protein pass from intestinal cells into lymphatic vessels. They travelfrom the lymph system to the blood stream where they circulate all over thebody to provide triglycerides to cells |
|
|
chylomicron remnants.
|
chylomicrons that have delivered dietaryfat to the body’s cells
Chylomicron remnants are taken up by the liver where they are converted tovery low density lipoproteins (VLDL). |
|
|
cholesterol is synthesized in the
|
liver
The liver packagescholesterol and triglycerides with protein into VLDL particles that thencirculate in the blood to deliver these lipids to cells of the body |
|
|
VLDL particles contain
|
~55-65% triglyceride, 10-15%cholesterol, and 5-10% protein.
|
|
|
As VLDL particles interact with enzymes in the bloodstream to give theirtriglycerides to cells, they are converted to
|
low density lipoproteins(LDL)
|
|
|
LDL particles contain
|
~45% cholesterol, 10% triglyceride, and 25% protein
|
|
|
LDL particles are the major carriers of____ in the bloodstream
|
cholesterol |
|
|
High circulating LDL is associated with increased risk of
|
atherosclerosis andheart disease, so LDL is often referred to as “bad cholesterol.”
|
|
|
remove LDL cholesterol from the blood and return it to the liver where itcan be reprocessed and incorporated into bile salts
|
High density lipoprotein (HDL)
|
|
|
high circulating levels of HDL are associated with reduced risk of
|
heart disease, HDL is often called “good cholesterol.”
|
|
|
Chylomicron
|
lipoprotein made in intestinal cells; delivers dietary fatto tissues after a meal
|
|
|
Chylomicron remnant
|
what’s left of a chylomicron after it hasdelivered dietary fatty acids to tissues
|
|
|
VLDL
|
triglyceride-rich lipoprotein made in the liver; deliverstriglycerides to tissues; gives rise to LDL
|
|
|
LDL
|
cholesterol-rich lipoprotein derived from VLDL remnants;delivers cholesterol to tissues
|
|
|
HDL
|
protein-rich lipoprotein made in the liver; delivers cholesterolfrom peripheral tissues back to the liver.
|
|
|
•Statin drugs
|
cholesterolmedication. Statins drugs act by blockingcholesterol synthesis in the liver.
|
|
|
The B-vitamin niacin sometimesprescribed to
|
lower LDL and raise HDL
|
|
|
bile acid resins
|
LDL-loweringmedication. work inthe small intestine to bind cholesterol inbile. Instead of being reabsorbed andreturned to the liver, the boundcholesterol is removed in feces.
|
|
|
Even when glycogen stores are adequate, many cells of the bodywill preferentially utilize
|
fat for fuel so that glycogen can be spared for thebrain and red blood cells
•RBCs lack mitochondria, the site of fatty acid oxidation, so they aredependent on glucose for fuel. •The blood-brain barrier precludes entry of fatty acids whereas glucose cancross the blood-brain barrier. |
|
|
fat mobilization
|
The process by which stored triglycerides are hydrolyzed to release glyceroland fatty acids into the bloodstream
|
|
|
In the cytoplasm of cells, glycerol is converted to
|
dihydroxyacetone phosphate (an intermediate in the glycolysispathway)Thus, glycerol can enter glycolysis as dihydroxyacetone phosphate to beconverted to pyruvate.Pyruvate can then be further catabolized for energy, or it can be converted toglucose by gluconeogenesis.
|
|
|
FA- The oxidation of fatty acids takes place in the
|
mitochondria of cells
|
|
|
FA- To move from the cytosol into the mitochondria, fatty acids must first be
|
“activated.”Activation involves conversion of the fatty acid into a molecule of fatty acylCoA.The reaction of a fatty acid with coenzyme A to form fatty acyl CoA is drivenby hydrolysis of a molecule of ATP.
|
|
|
FA- An activated fatty acid that enters the mitochondria is broken down by aprocess called
|
β-oxidation. the pathway by which a molecule of fatty acyl CoA is brokendown into molecules of acetyl-CoA.
|
|
|
β-oxidation pathway
|
β-oxidation begins with the oxidation of the 2nd carbon atom (i.e., theβ-carbon) of the fatty acyl CoA molecule. A 2-C unit is removed from the fattyacyl CoA and converted to a 2-C molecule of acetyl CoA. Consequently, the fattyacyl CoA molecule is now 2 carbons shorter.•The entire process repeats, resulting in the cleavage of another 2-C moleculethat becomes acetyl CoA.•This repeats again and again. (Hence, the overall process is sometimes called a“spiral.”)•NAD+ and FAD function as electron carriers.•Every run through the spiral produces a molecule of acetyl CoA, a molecule ofNADH, and a molecule of FADH2 until the remaining fatty acyl CoA is only 4-Clong.•The final pass through the spiral produces 2 final acetyl CoA molecules.Hence, the products of beta-oxidation are: acetyl CoA, FADH2, NADH, and H+
|
|
|
β-oxidation of one fatty acid results in formation of
|
many acetylCoA molecules
Each acetyl CoA can enter the citric acid cycle and then the electrontransport chain to yield several molecules of ATP.The NADH and FADH2 from β-oxidation can also enter the electron transportchain to yield ATP. oxidation of fatty acids yield much more energy (ATP) compared tooxidation of glucose |
|
|
first step of the citric acid cycle occurs when
|
a molecule ofacetyl CoA combines with a molecule of oxaloacetate to form citrate
|
|
|
Under certain conditions, β-oxidation of fatty acids can produce acetyl CoAmolecules faster than they can
|
enter the citric acid cycle. (For example, whenglucose availability is low, oxaloacetate will be converted to glucose bygluconeogenesis leaving less oxaloacetate available for the citric acid cycle.)
|
|
|
When the amount of acetyl CoA molecules produced by β-oxidation exceedsthe capacity of the citric acid cycle, acetyl CoA is converted to
|
ketone bodiesin the liver.
|
|
|
3 different ketone bodies
|
acetone, acetoacetate, and β-hydroxybutyrate.
|
|
|
ketogenesis
|
formation of ketone bodies |
|
|
ketosis |
high amount of ketone bodies in the blood |
|
|
Ketonuria
|
the presence of ketone bodies in the urine.
|
|
|
Ketoacidosis
|
low blood pH due to elevated levels of ketone bodies. leading to coma or death
|
|
|
Diabetic Ketoacidosis (DKA)
|
condition that can occur in type I diabetics. Eventhough blood glucose levels are abnormally high, glucose cannot enter cells to be oxidized for fuelwithout insulin. Unable to use glucose for fuel, the body catabolizes excessive fatty acids.Production of acetyl CoA exceeds the capacity of the citric acid cycle, resulting in ketogenesis.Buildup of acidic ketone bodies leads to ketoacidosis.
|
|
|
Fatty acid synthesis
|
excess energy intake can lead to fatty acid biosynthesis and storageof fat in adipocytes.
|
|
|
Biosynthesis of fatty acids from non-fat substrates takes place in the
|
cytoplasm of several different types of cells. (e.g., cells of the liver, adiposetissue, central nervous system, and mammary glands)
|
|
|
Endogenous synthesis of fatty acids begins with
|
acetyl CoA
|
|
|
De novo synthesis of fatty acids entails the combining of eight acetyl groups(2-C units from acetyl CoA) to form a 16-C saturated fatty acid called
|
palmitate.
Palmitate can be elongated or desaturated to form other fatty acids. |
|
|
acetyl CoA can be produced from
|
glucose (through pyruvate), aminoacids, and fatty acids. Thus, excess dietary intake of carbohydrate, protein, and/orfat can all lead to de novo synthesis of fatty acids and consequent accumulation ofbody fat.
|
|
|
the pyruvate dehydrogenase reaction that converts pyruvate toacetyl CoA is not reversible.
|
Thus, glucose can be converted to acetyl CoA, butacetyl CoA cannot be converted to glucose. So, the body can convert glucose tofatty acids, but it cannot convert fatty acids to glucose.Glucose ↔ pyruvate → acetyl CoA ↔ fatty acids
|
|
|
Excess amino acids not used for protein synthesis are
|
degraded
they cannot be stored like glycogen andtriglycerides. |
|
|
Protein turnover
|
continuing process of protein breakdown and proteinsynthesis in the body
|
|
|
The amino acid pool
|
the total supply of amino acids in the body
|
|
|
Amino acids in body can come from:
|
•proteins ingested in the diet
•breakdown of the body’s proteins •synthesis of nonessential amino acids in the liver |
|
|
The nitrogen from degraded amino acids is either:
|
•Used to synthesize other nitrogen-containing molecules, or Eliminated from the body in the urine
|
|
|
The 3 stages of nitrogen catabolism are:
|
1. Transamination
2. Deamination 3. Urea formation |
|
|
Transamination
|
the transfer of an amino group from one molecule to another
|
|
|
Transaminases
|
enzymes that catalyze the transfer of amine groups
|
|
|
two key amino acids in catabolism of other amino acids
|
Aspartate and glutamate.
specific examples of transamination |
|
|
Deamination
|
removal of an amine functional group from an amino acid
The resulting ammonia (NH3) or ammonium ion (NH4+) enters the urea cycle. |
|
|
The Urea Cycle
|
a metabolic pathway in which ammonia is converted to urea.
Ammonia is toxic, so it must beremoved from the body.By the urea cycle, ammonia isconverted to urea.Urea is less toxic than ammonia, soit can circulate in the blood until it isremoved by the kidneys |
|
|
The urea cycle takes place in the
|
liver
After the formation of urea in the liver, urea diffuses into the blood The kidneys filter blood and excrete urea in the urine |
|
|
Blood urea nitrogen (BUN)
|
common blood test todetermine the amount of nitrogen that is present insomeone’s blood as urea.
An elevated BUN may be a sign of renal impairment. |
|
|
liver failure and ammonia |
People with liver failure may not be able to properly process ammonia tourea, leading to elevated blood levels of ammonia.Because ammonia is toxic to the central nervous system, a brain dysfunctioncalled hepatic encephalopathy may result.Signs and symptoms of mild hepatic encephalopathy may include confusionor changes in behavior. Severe hepatic encephalopathy can lead to comaand death.
|
|
|
Amino acid catabolism
The carbon skeleton of amino acids can be: |
• Used for ATP production -The carbon skeleton of some amino acids may be converted to pyruvate,others to acetyl CoA, and still others to one of the intermediates of thecitric acid cycle to be oxidized for energy.
•Used to synthesize glucose by gluconeogenesis•Converted to fatty acids for triglyceride storage in adipose tissue |
|
|
After the amine group of an amino acid is removed, the remaining carbonskeleton can be converted to
|
pyruvate, acetyl Co A, or one of severalintermediates of the citric acid cycle.
carbon skeletons from all 20 amino acids can be catabolized forenergy production |
|
|
Pyruvate and oxaloacetate can serve as precursors for synthesis of glucose bygluconeogenesis. Thus, carbon skeletons that are degraded to pyruvate (or citricacid cycle intermediates that produce oxaloacetate) can be converted to glucose.Amino acids with carbon skeletons that can be converted to glucose are called
|
glucogenic amino acids.
|
|
|
Carbon skeletons that are degraded to acetyl CoA (or its precursor, acetoacyl CoA)are not glucogenic. (Acetyl CoA cannot form pyruvate or oxaloacetate because thepyruvate dehydrogenase reaction that converts pyruvate to acetyl CoA is notreversible). Although acetyl CoA cannot be converted to glucose, it can be used tomake ketone bodies. Thus, amino acids with carbon skeletons that are convertedto acetyl CoA are called
|
ketogenic amino acids
|
|
|
both glucose and acetyl CoA can be converted to
|
fattyacids. So, although the body cannot store amino acids, excess energyintake from amino acids can result in fatty acid synthesis andconsequent fat storage.
|
|
|
summary of overall carbon-skeleton metabolism:
|
•If the body needs energy, the carbon skeleton of amino acids canbe oxidized for energy via the citric acid cycle.
•If carbohydrate is lacking in the diet (or in the case diabetes whenglucose cannot enter cells), glucogenic amino acids are convertedto pyruvate or oxaloacetate to be used to gluconeogenesis. •If excess protein in the diet provides excess energy, the carbonskeletons will be used for synthesis and storage of fat. |
|
|
Amino acid biosynthesis
|
11 amino acids can be synthesized de novo by the body. |
|
|
9 essential amino acids |
Valine, Methionine, Histidine,Leucine, Phenylalanine, Lysine, Threonine, Tryptophan, Isoleucine
they cannot besynthesized by the body in adequate amounts |
|
|
intermediates of the glycolysis pathway andcitric acid cycle serve as starting materials for
|
synthesis of 9 non-essentialamino acids.
|
|
|
The non-essential amino acid tyrosine has a unique structure
|
tyrosine has anaromatic side chain.
|
|
|
The precursor for endogenous tyrosine synthesis is theessential amino acid
|
phenylalanine
|
|
|
Yeast ferments carbohydrates such as sugars and starch to
|
ETOH |
|
|
2010 Dietary Guidelines for ETOH
|
“If alcohol is consumed, it should be consumed in moderation--up toone drink per day for women and two drinks per day for men--andonly by adults of legal drinking age.”• In the United States, a “standard drink” is equal to 14.0 grams (0.6 ounces)of pure alcohol.
• This is approximately the amount in 12 oz of beer, 5 oz of wine, or 1.5 oz of 80-proof distilled spirits. |
|
|
Absorption of ethanol
|
•Unlike the macronutrients, ethanol does not need to be digested to smaller endproducts to be absorbed.
•Unlike macronutrients which are absorbed exclusively in the small intestine, alcoholcan also be absorbed in the stomach, so blood alcohol levels will begin to rise withinminutes of ingestion. •A variety of factors can influence the rate of absorption. For instance, whetheralcohol is consumed with food as well as the type and amount of food will affectethanol’s rate of absorption. Absorption and metabolism differ between genders. For a givenamount of alcohol, women tend to have a higher blood alcoholconcentration than men. This is partly due to the smaller size andlower total body water of women. However, women have loweractivity of a stomach enzyme that metabolizes alcohol, allowingfaster absorption of ingested alcohol into the blood.In any case, ethanol is always metabolized muchmore slowly than it is absorbed. |
|
|
Intoxication from ethanol
|
Ethanol is a unique chemical structure in that it is both water soluble and lipid soluble.
Its lipophilic properties allow some ethanol to pass directly from the bloodstream to thebrain where ETOH acts as a central nervous system depressant.Ethanol acts at many sites in the brain, including the reticular formation, cerebrum,and cerebellum.Ethanol also affects the activity of several neurotransmitters including the principleinhibitory neurotransmitter gamma-aminobutyric acid (GABA).Chronic heavy consumption of alcohol can alter brain chemistry so that a person maypresent with severe withdrawal symptoms when alcohol is stopped. Symptoms ofwithdrawal may include tremors, rapid breathing and pulse, spikes in blood pressure,hallucinations, and seizures. |
|
|
legal systems typically define “intoxication” as bloodalcohol concentration (BAC)
|
0.08 - 0.1g/100ml.
|
|
|
BAC of 0.3 g/100ml or greater can lead to
|
coma or death.•Death by ethanol toxicity may result from a variety of overlappingfactors, including depression of respiratory centers in the brainstem,metabolic acidosis, or even multi-system organ failure.
|
|
|
Ethanol is broken down in the
|
liver by a series of oxidation reactions.
•The first step takes place in the cytoplasm when the enzyme alcoholdehydrogenase catalyzes the conversion of ethanol toacetylaldehyde.Acetylaldehyde can condense with amino groups of nucleic acids andproteins, causing damage to cells. •Because, acetaldehyde is highly toxic, it is quickly metabolized toacetyl CoA by the enzyme acetaldehyde dehydrogenase.This step takes place in mitochondria of the liver. |
|
|
In the metabolism of ETOH, NAD+ is reduced to
|
NADH
NAD+ acts as an electron acceptorin the oxidation reactions of ethanol metabolism.Thus, when ethanol is oxidized, NAD+ is reduced to NADH. |
|
|
The end products of ethanol metabolism are
|
acetyl CoA, NADH, CO2, and H2O
|
|
|
Alcohol and diabetes
|
Upon ingestion of ethanol, the liver prioritizes its metabolism above all else,including gluconeogenesis and glycogenolysis.Thus, diabetics on insulin or oral hypoglycemic medications should practiceextra caution with alcohol to avoid dangerous hypoglycemia.The American Diabetes Association recommends that diabetics never drink onan empty stomach, drink only in moderation (a maximum of two drinks per dayfor men and one for women), and always have glucose tablets or anothersource of simple sugar on hand.
|
|
|
The acetyl CoA produced from the oxidation of ethanol can
|
enter the citricacid cycle to be oxidized for energy, or it can be used for fatty acidbiosynthesis.NADH can enter the electron transport chain for ATP production.ETOH is a more concentrated source of energy than carbohydrate.It provides 7 kcals/g compared to 4 kcals/g for CHO.
|
|
|
Altered liver metabolism by heavy ethanol consumption:
|
Heavy ethanol consumption leads to an accumulation of NADH, which inturn, disrupts normal liver metabolism:•High concentrations of NADH favor the conversion of pyruvate tolactate. Buildup of lactic acid may disrupt acid/base homeostasis.•Excessive acetyl CoA can also lead to the formation of acidic ketone bodieswhich worsen acidosis.•High concentrations of NADH inhibit fatty acid oxidation and stimulatefatty acid biosynthesis.•Accumulation of triglycerides in the liver can result in steatosis (“fatty liver”).
|
|
|
At moderate concentrations, ethanol is metabolized by
|
alcoholdehydrogenase
|
|
|
large doses of ETOH invoke a pathway called the
|
MicrosomalEthanol Oxidizing System (MEOS) in the endoplasmic reticulum of the liver.•This pathway does not result in the production of ATP, but it is the body’sattempt to eliminate dangerous acetylaldehyde.•Breakdown of alcohol by the ethanol-oxidizing pathway also generatesmany reactive oxygen species (ROS).
|
|
|
Ethanol tends to increase estradiol concentrations in women.
|
•This may be beneficial to reduce risk of osteoporosis andcardiovascular disease.•However, it also poses increased risk for women with a family historyof breast cancer.
|
|
|
•Ethanol inhibits secretion of
|
antidiuretic hormone from the pituitary, soit negatively impacts fluid balance.
|
|
|
FrenchParadox
|
light-moderatealcohol consumption is associated with reduced risk or cardiovascular disease
The benefits may be mediated through increased HDL, decreased oxidation of LDL,anticoagulant properties, and reduction of plasma homocysteine.Interestingly, the relationship between alcohol intake and cardiovascular disease risk appears tobe a J-shaped curve. This indicates that lowest risk is associated with light-moderateconsumption; however, the dose-response relationship is such that higher intakes areassociated with increased risk.The article also cites studies relating binge drinking patterns to hypertension and increased risk.The authors conclude that evidence for cause-and-effect is not strong enough to recommendthat non-drinkers take up drinking. It is important to keep in mind that epidemiological studiesare large population studies designed to identify correlations between environmental exposuresand disease risk. Epidemiological studies do not establish causality, and the relationshipbetween exposure and risk may differ from person to person.•However, taken as a whole, existing evidence suggests that light-moderate alcoholintake may be cardioprotective |
|
|
Fetal Alcohol Syndrome
|
The liver of a fetus does not contain the enzymes necessary to breakdown ethanol, so ethanol that crosses the placenta and enters the fetuscan lead to deformities and mental retardation
|
|
|
Alcoholic liver disease
|
Alcoholic liver disease progresses in 3 stages:•Steatosis•Alcoholic hepatitis•Cirrhosis
|
|
|
Steatosis (i.e., fatty liver)
|
occurs when fat accumulates in the liver.Normally, fatty acids serve as the main source of fuel for the liver. Whenalcohol replaces fatty acids as the liver’s main source of energy, unused fattyacids accumulate as triglyceride in the liver.•Steatosis is reversible by reducing alcohol consumption.
|
|
|
Alcoholic hepatitis
|
is characterized by inflammation and swelling of the liver.
•This condition can produce irreversible damage and can even be fatal. |
|
|
cirrhosis
|
dying liver cells are replaced by fibrous scartissue.• A cirrhotic liver is unable to remove toxins from the blood, regulate carbohydratemetabolism, synthesize hepatic proteins, or convert ammonia to urea. Althoughdiet and lifestyle changes may ameliorate some of the symptoms of cirrhosis, thedamage is irreversible, and a liver transplant is often the only treatment option.
|
|
|
Alcoholics are prone to micronutrient deficiencies due to
|
poor diet andinterference of alcohol with nutrient absorption and metabolism
|
|
|
Alcoholic patients frequently present with
|
electrolyte imbalances,acid/base abnormalities, and anemia.
These multiple, overlappingimbalances in homeostasis can create complex medical cases |
|
|
rally pack/banana bags
|
intravenous solutionsometimes given in the hospital to correct nutrientdeficiencies in a patient.
commoncomponents are multi-vitamins (MVI), folic acid,thiamine, and magnesium sulfate, prepared in a sterilesaline solution. |
