Term
| What is the purpose of food intake, digestion, & absorption? |
|
Definition
| Supply of food mol's (Glc, aa, FAs) |
|
|
Term
| What is the fate of food mol's? |
|
Definition
| Energy to sustain life processes; Storage; Building Blocks |
|
|
Term
| Give examples of food mol's as energy to sustain life processes. |
|
Definition
| Active Transport; Synthesis/Replication; Contractions; Heat Production/Thermoregulation |
|
|
Term
| Give examples of food mol's as storage. |
|
Definition
| Fat; Glycogen; Protein Pool |
|
|
Term
| Give examples of food mol's as building blocks. |
|
Definition
| Membranes; Muscle Proteins; Hormones |
|
|
Term
| What does the main direction of metabolism depend on? |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| How many C is acetyl group? |
|
Definition
|
|
Term
| How many C is carbon dioxide? |
|
Definition
|
|
Term
| What are the main directions of metabolism? |
|
Definition
| Energy Storage (Anabolic); Energy Mobilization (Catabolic); Conversions |
|
|
Term
| How are fuel stores interconnected? |
|
Definition
| "Spinal Column" of C compounds by a multitude of p'ways |
|
|
Term
| What are the directions of metabolic p'ways controlled by? |
|
Definition
| Hormones; NS; ATP/ADP Formation; Accumulation of intermediates/end-products |
|
|
Term
| When is hyperglycemia normal? |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Glc is the _____ fuel in all tissues, but the _____ fuel in _____ tissues. |
|
Definition
| Preferred; Essential; Glc-dependent |
|
|
Term
| Give some examples of Glc-dependent tissues. |
|
Definition
| NS, RBCs, Retina, Renal Medulla, Gonads, Fetus, Lactation |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| Below normal glucose levels --> _____ |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| What tissue suffers 1st in hypoglycemia? |
|
Definition
|
|
Term
| How is maintenance of blood Glc levels achieved? |
|
Definition
| Via eating/digesting/absorbing Glc; Storing (glycogenesis) & Releasing stored Glc (Glycogenolysis); Synthesis of new Glc from precursors (Gluconeogenesis) |
|
|
Term
| What tissue is the greatest consumer of Glc? |
|
Definition
|
|
Term
| What hormone(s) combat(s) hypoglycemia? |
|
Definition
| Glucagon, Cortisol, Epinephrine |
|
|
Term
| What hormone(s) combat(s) hyperglycemia? |
|
Definition
|
|
Term
| How does Glc enter cells? |
|
Definition
|
|
Term
| FD is ______-dependent & req's _____. |
|
Definition
| Concentration; Glc Transporters (GLUTs) |
|
|
Term
| Is the liver Glc-dependent? |
|
Definition
|
|
Term
| What tissues have GLUTs as part of their cm? When is FD active? |
|
Definition
| Glc-dependent tissues + Liver; Always |
|
|
Term
| What tissues have GLUTs stored intracellularly? When is FD active? |
|
Definition
| Glc-independent tissues (m., fat); Only when insulin present |
|
|
Term
| What is secreted in response to hyperglycemia? What does this allow? |
|
Definition
| Insulin; Fusion of GLUTs w/ cm |
|
|
Term
| In hyperglycemia, what cells have access to blood Glc? |
|
Definition
|
|
Term
| In hypoglycemia, what cells have access to blood Glc? |
|
Definition
|
|
Term
| In hypoglycemia, what do Glc-independent cells use for fuel? |
|
Definition
|
|
Term
| Glc Trapping: ____. Is it reversible? |
|
Definition
| Upon cell entry, Glc is phosphorylated to G6P; Glc can't diffuse out of cells; Irreversible except in liver, kidney, & GI cells |
|
|
Term
| Can G6P pass through GLUTs? |
|
Definition
|
|
Term
| What does the fate of Glc depend on? |
|
Definition
|
|
Term
| Describe energy gain from Glc in aerobic conditions. |
|
Definition
| Glycolysis --> Acetyl CoA --> Krebs Cycle --> ETC |
|
|
Term
| Describe energy gain from Glc in anaerobic conditions. |
|
Definition
| Glycolysis & Lactic Acid formation |
|
|
Term
| Describe energy storage of Glc. |
|
Definition
| Glycogen; Conversion of Glc into FAs |
|
|
Term
| Where does glycolysis occur? |
|
Definition
|
|
Term
|
Definition
| Splitting of a C6 into 2 C3 (Pyruvates) |
|
|
Term
| What is the purpose of glycolysis? |
|
Definition
| Prepare Glc for entry into Mt; Some ATP (2/Glc) generated; Some of Glc's chemical energy transferred/stored via H in form of NADH/H+ for entry into ETC |
|
|
Term
| After glycolysis, pyruvate enters _____ (structure). |
|
Definition
|
|
Term
| What happens to pyruvate in Mt? |
|
Definition
| Decarboxylated to acetyl group; Acetyl group attaches to Coenzyme A (Acetyl CoA) which is ready to enter Krebs Cycle |
|
|
Term
| Where does the Krebs Cycle occur? |
|
Definition
|
|
Term
| What is another name for the Krebs Cycle? |
|
Definition
|
|
Term
|
Definition
| Sequence of rxn's in which Acetyl group is degraded to 2 CO2, 1 ATP, 8 H atoms (NADH/H+) |
|
|
Term
| Acetyl CoA combines w/ ____ to form ____ in Krebs Cycle. |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| What happens to Citric Acid in the Krebs Cycle? |
|
Definition
| Undergoes a sequence of decarboxylations & dehydrations ending again in OAA |
|
|
Term
| What does the Krebs Cycle start & end w/? |
|
Definition
|
|
Term
| What is the most important outcome of Glc oxidation in the Krebs Cycle? |
|
Definition
| Making energy-rich H ions available for subsequent oxidation in ETC |
|
|
Term
|
Definition
|
|
Term
| In addition to its most important function, what is the Krebs Cycle involved in? |
|
Definition
Synthesis & Combustion of FA & aa
Synthesis of Glc |
|
|
Term
|
Definition
| Series of e- carriers integrated into inner Mt membrane, in which the energy stored in NADH/H+ is transferred to ATP |
|
|
Term
| What is another name for ETC? |
|
Definition
| Oxidative Phosphorylation |
|
|
Term
| What does Ox Phos lead to? |
|
Definition
| Generation of ATP, Regeneration of NAD, Formation of H2O out of remaining protons & O2 |
|
|
Term
|
Definition
| Glycolysis & Citric Acid Cycle |
|
|
Term
| Describe what happens to carbohydrates in anaerobic conditions/what would happen w/o anaerobic metabolism. |
|
Definition
| Lack of O2, NADH/H+ pile up, reduce Krebs Cycle activity (product inhibition), Pyruvate will pile up/could inhibit glycolysis, ATP production would seize totally |
|
|
Term
| What must happen to keep glycolysis open in anaerobic conditions? |
|
Definition
| Pyruvate must be removed & NAD regenerated via Lactate |
|
|
Term
| What reduces pyruvate to lactic acid? |
|
Definition
|
|
Term
| What does Lactate Dehydrogenase do? Why is this important? |
|
Definition
| Reduces Pyruvate to Lactic Acid, thus regenerating NAD; Some ATP can still be generated via anaerobic glycolysis |
|
|
Term
| What is the main energy p'way in RBCs? |
|
Definition
|
|
Term
|
Definition
| Must be removed; Diffuses rapidly into circulation; Utilized by tissues when O2 available (heart m), where LDH converts it back to pyruvate --> aerobic p'way; Enters Gluconeogenesis in liver to produce new Glc |
|
|
Term
|
Definition
|
|
Term
|
Definition
| Muscle, Liver, RBCs, GI tract, Kidneys |
|
|
Term
| How does tissue damage relate to LDH? |
|
Definition
| Tissue Damage --> Leakage of LDH into plasma --> Diagnostic Significance |
|
|
Term
| What are 2 events that can lead to increased plasma LDH? |
|
Definition
| Hemolysis & Muscle injury |
|
|
Term
| What happens if excess Glc is available? |
|
Definition
| Stored in liver & m. as glycogen (glucose polymer) for later use (Glycogenesis) |
|
|
Term
| What is the advantage of glycogenesis? |
|
Definition
| Glycogen precipitates & is not osmotically active |
|
|
Term
| What are the main glycogen storing organs? Max %? |
|
Definition
|
|
Term
| When sm Glc-chains have formed in alpha-1-4 linkages, what transfers groups of 6 Glc units as side chains in alpha-1-6 linkages? What does this form? |
|
Definition
| Branching enzyme; Branched carbohydrate |
|
|
Term
| What happens if Glc is needed for energy? |
|
Definition
| Glycogen broken down to G6P (Glycogenolysis) |
|
|
Term
| What is req'd for Glycogenolysis? |
|
Definition
|
|
Term
| What is req'd to release free Glc from G6P into circulation? |
|
Definition
|
|
Term
| Where is phosphatase present? |
|
Definition
| Liver & Kidney cells (Not muscle cells) |
|
|
Term
| What does hepatic glycogenolysis do? |
|
Definition
| Increases blood Glc levels |
|
|
Term
| What does muscle glycogenolysis do? |
|
Definition
| Increases muscle energy supply |
|
|
Term
| What stimulates glycogenesis? What stimulates glycogenolysis? |
|
Definition
| Insulin; Glucagon, Cortisol, Epi |
|
|
Term
| How does Glc diffuse out of the liver? |
|
Definition
|
|
Term
| What happens when blood Glc runs low & Glycogen stores are exhausted? |
|
Definition
| Glc must be synthesized to supply Glc-dependent tissues (Gluconeogenesis) |
|
|
Term
| Where does Gluconeogenesis occur? |
|
Definition
|
|
Term
| What are precursors of Gluconeogenesis? |
|
Definition
| Many aa's, Lactate, Propionate from fermentation, Glycerol from triglyceride breakdown |
|
|
Term
| What happens to precursors of Gluconeogenesis? What is an exception? |
|
Definition
| Enter Krebs Cycle & are pulled into cytoplasm as OAA/Malate to enter Gluconeogenesis; Glycerol |
|
|
Term
| Both ____ & ____ contain phosphatases & release _____ into circulation. |
|
Definition
|
|
Term
| What % of Gluconeogenesis is the Liver responsible for? Kidney? |
|
Definition
|
|
Term
| Dietary fats consist mostly of: |
|
Definition
| Triglycerides, Phospholipids, Cholesterol |
|
|
Term
| What are lipids utilized for? |
|
Definition
| Energy gain, Energy storage for later use, Building blocks (membranes), Hormones & Bile acids |
|
|
Term
| Are lipids hydrophilic or hydrophobic? |
|
Definition
|
|
Term
| Lipids must be made ____ for transport in plasma. |
|
Definition
|
|
Term
| How are lipids made soluble for transport? |
|
Definition
| Combining w/ proteins --> Lipoproteins |
|
|
Term
|
Definition
| Aggregations of lipids surrounded by a shell of hydrophilic proteins, phospholipids, & specific R proteins (Apoproteins) |
|
|
Term
| What are the 2 classes of lipoproteins? (What are they formed by?) |
|
Definition
| Chylomicrons (Sm intestinal enterocytes after absorption of lipids); VLDLs (liver cells after production of new lipids) |
|
|
Term
|
Definition
| Very Low Density Lipoprotein |
|
|
Term
| What do Chylomicrons/VLDLs do? |
|
Definition
| Circulate; their Apoproteins bind endothelial R's & activate endothelial LPLs |
|
|
Term
|
Definition
|
|
Term
|
Definition
| Dissolve shells of Lipoproteins & Hydrolyze Triglycerides --> FFAs + Glycerol Diffuse into respective tissues for Storage or Energy |
|
|
Term
| What is the fat storage form of lipids? How is this storage accomplished? |
|
Definition
| Triglycerides; After diffusion into Adipocytes, triglycerides reform |
|
|
Term
|
Definition
|
|
Term
| When is lipolysis initiated? |
|
Definition
| When circulating fuel levels (Glc) are low & Energy is needed |
|
|
Term
|
Definition
| HSL hydrolyzes stored triglycerides --> FFAs & Glycerol diffuse back into circulation; FFAs bind to plasma Albumin for transport = NEFAs, which deliver FFAs to tissues for energy gain |
|
|
Term
|
Definition
|
|
Term
| In fat tissues, insulin stimulates _____ & inhibits _____. (substances) |
|
Definition
|
|
Term
| What does binding of FFAs to Albumin prevent? |
|
Definition
|
|
Term
| How do FFAs & Glycerol diffuse into circulation? |
|
Definition
| Down a concentration gradient |
|
|
Term
| What is a Non-Esterified FA? |
|
Definition
|
|
Term
| What does HSL respond to? |
|
Definition
| Insulin, Glucagon, Cortisol, Epi, etc. |
|
|
Term
| Is fat stored in muscle cells? How do muscle cells access FFAs? What do they use them for? |
|
Definition
| No; Chylomicrons, VLDLs, NEFAs; Energy |
|
|
Term
| How are FFAs utilized for energy gain? |
|
Definition
| By entering Beta-Oxidation, which releases Acetyl groups for use in the Krebs Cycle/ETC |
|
|
Term
| Where can FFAs originate from? |
|
Definition
| NEFAs, VLDLs, Chylomicrons |
|
|
Term
| What do FFAs do after entering a cell? |
|
Definition
| Enter Mt & undergo progressive release of C2 segments as Acetyl CoA = Beta Oxidation |
|
|
Term
| What happens to Acetyl CoA from Beta oxidation? |
|
Definition
| Enters Krebs Cycle for complete oxidation & ATP generation in ETC |
|
|
Term
| Where does Glycerol diffuse? |
|
Definition
|
|
Term
| What happens to Glycerol after it diffuses into active tissues? |
|
Definition
| Can enter Glycolysis --> Krebs Cycle --> ETC when ATP is needed; or enter Gluconeogenesis when Glc is needed |
|
|
Term
| What is Glycerol an intermediate of? |
|
Definition
|
|
Term
| d/o ______, Glycerol can either _____ or _____. |
|
Definition
| Which Hormones are present; --> Energy production; --> Gluconeogenesis |
|
|
Term
|
Definition
| Making new fat out of excess energy; Excess Glc & aa's can be converted into FFAs |
|
|
Term
| Where does Lipogenesis occur? |
|
Definition
| Liver, Fat Tissue, Mammary Gland |
|
|
Term
| When is lipogenesis activated? |
|
Definition
| When stores of ATP, Glycogen, & Labile Protein are full & Glc & aa's are still available |
|
|
Term
| What happens in Lipogenesis? |
|
Definition
| FFAs are condensed into TGs for storage (adipocytes only) or secreted into milk |
|
|
Term
| Is the liver a fat storage site? |
|
Definition
|
|
Term
| Describe the Liver's role in Lipogenesis. |
|
Definition
| Packs newly produced TGs into Lipoproteins = VLDLs --> Exocytosis into circulation --> Fat Tissue LPLs hydrolyze VLDLs --> Fat storage |
|
|
Term
| What stimulates Lipogenesis? |
|
Definition
|
|
Term
| What does the Liver do during Lipolytic phases? |
|
Definition
| Readily takes up FFAs from NEFAs w/o utilizing all for energy (acts like a "fat sponge"); Makes FFAs from NEFAs available to other tissues as VLDLs & Ketone Bodies |
|
|
Term
| What is the advantage of VLDL formation? |
|
Definition
| Albumin binding capacity for FFA is limited --> Liver increases lipid transport capacity via VLDLs |
|
|
Term
|
Definition
| Many FFAs are resynthesized into TGs & packaged into VLDLs which are released into circulation & taken up by tissues via their endothelial LPLs for energy gain via beta oxidation |
|
|
Term
| Is insulin present in lipolytic phase? |
|
Definition
|
|
Term
|
Definition
| Acetyl groups condensed into Acetoacetic Acid, Acetone, & Beta-Hydroxybutyrate; A physiological & very important energy source for many tissues when Glc levels are low |
|
|
Term
| Many FFAs enter B-Oxidation & _____ accumulates. |
|
Definition
|
|
Term
| Why does Acetyl CoA accumulate in B-Oxidation? |
|
Definition
| as liver ATP stores fill, Krebs Cycle activity declines; OAA/Malate are withdrawn from Krebs Cycle for Gluconeogenesis |
|
|
Term
| What happens to accumulating Acetyl CoA groups from B-Oxidation? |
|
Definition
| Condense into Ketone Bodies |
|
|
Term
| What is another name for Ketone Bodies? |
|
Definition
|
|
Term
| Is hepatic KB formation reversible? |
|
Definition
|
|
Term
| Where are hepatic KBs released? What happens to them? |
|
Definition
| Into blood --> Taken up by other tissues --> Hydrolyzed back to Acetyl CoA --> Enter Krebs Cycle/ETC for energy gain |
|
|
Term
| What is an advantage of KB formation? |
|
Definition
| Liver B-oxidizes FFA for other tissues & supplies an easily usable hydrophilic substrate for energy gain, e.g. to neurons & mm. |
|
|
Term
| What % of body solids are proteins? |
|
Definition
|
|
Term
| What are 2 types of proteins? |
|
Definition
| Essential & Non-essential aa |
|
|
Term
| What are the functions of proteins? |
|
Definition
| Structural components, Contractile elements, Transporters, Enzymes & Hormones, Hemostatic Factors, Ab's |
|
|
Term
| How many aa are essential? |
|
Definition
|
|
Term
|
Definition
|
|
Term
| How are aa absorbed from circulation? |
|
Definition
| FD or AT (into liver & m.) |
|
|
Term
| Describe what happens after aa's are absorbed from circulation. |
|
Definition
| Cell entry --> Peptides + Proteins are formed = Labile Protein Pool = Temporary storage form |
|
|
Term
| What is the function of the Labile Protein Pool? |
|
Definition
| Temporary Storage Form/no function |
|
|
Term
| What happens to the Labile Protein Pool? |
|
Definition
| Rapid Proteolysis possible via lysozomal enzymes --> constant turnover btw plasma aa's/pool; Functional proteins are formed out of Labile pool |
|
|
Term
| What is alpha-ketoglutarate? |
|
Definition
| An intermediate of the Krebs Cycle |
|
|
Term
| When are most aa's metabolized? |
|
Definition
| After deamination to Keto-Analogs |
|
|
Term
| Describe deamination of aa's. |
|
Definition
| Removal of amino group to their respective keto-analog (reversible) |
|
|
Term
| What is the keto-analog of Alanine? |
|
Definition
|
|
Term
| What is the keto-analog of Glutamate? |
|
Definition
|
|
Term
| What happens to Keto-analogs? |
|
Definition
| Enter p'ways of Carbohydrate metabolism |
|
|
Term
| What are the 5 options of keto-analogs in carb metabolism? |
|
Definition
| Enter Krebs cycle for energy gain; Enter KC & are drawn out as Malate/OAA for gluconeogenesis; Enter KC & are shunted via Citrate into Lipogenesis; Form KBs via excess acetyl coA; intermediates leave KC for amination to NEFAs |
|
|
Term
| In which option for keto-analogs is the amino group utilized? |
|
Definition
| Amination to NEFAs (Detox) |
|
|
Term
| What keto-analog is a key branching point of metabolism? |
|
Definition
|
|
Term
| Deamination of aa to keto analogs involves release of _____. |
|
Definition
|
|
Term
| Where are the amino groups released during deamination transferred? |
|
Definition
| To alpha-ketoglutarate to form Glutamate, or to Pyruvate to form Alanine |
|
|
Term
| After amino groups are transferred to keto-analogs, what happens? |
|
Definition
| Glutamine/Alanine then transfer amino groups to other compounds (e.g. aa synthesis), which involves various amino-transferases |
|
|
Term
| Where are amino transferases found? |
|
Definition
|
|
Term
| Name 2 amino-transferases. What value do they serve? |
|
Definition
| ALT (Alanine at) & AST (Aspartate at); Increase in plasma levels of these enzymes are of diagnostic value |
|
|
Term
| What happens to excess amino groups that are not needed? |
|
Definition
| Liver converts excess potentially toxic ammonia to Urea --> Renal excretion |
|
|
Term
|
Definition
| Accumulation of NH3 (due to liver failure) --> Interference w/ GABA a/o Glutamate NTs --> Neurotoxicity --> Depression, Neurological Deficits, Coma, Death |
|
|
Term
| What does accumulation of NH3 do to GABA? |
|
Definition
| Enhances its function (which is inhibitory) |
|
|
Term
| What are some signs of hepatic encephalopathy? |
|
Definition
| Uncontrolled pacing, circling, lethargy, depression, neurological deficits, coma, death |
|
|
Term
| Where is ALT present? AST? |
|
Definition
|
|
Term
| What amino-transferase is liver-specific in sm animals? |
|
Definition
|
|
Term
| ALT increases in parallel to ______. |
|
Definition
|
|
Term
|
Definition
|
|
Term
| What is the detox product of ammonia? |
|
Definition
|
|
Term
| What happens to dietary carbs in ruminants? |
|
Definition
| Essentially all fermented to VFAs (Acetate, Butyrate, Propionate) |
|
|
Term
| In ruminants, how much Glc/maltose reaches the SI for absorption? |
|
Definition
|
|
Term
| What are the basic Glc demands in ruminants compared to monogastrics? |
|
Definition
| The same or Higher, e.g. during lactation |
|
|
Term
| Ruminants are potentially _____. |
|
Definition
|
|
Term
| What do ruminants depend on to maintain adequate blood Glc levels? |
|
Definition
| Gluconeogenesis (entirely) |
|
|
Term
| Describe gluconeogenesis in ruminants. |
|
Definition
| Always switched on; Provides 90-100% of Blood Glc |
|
|
Term
|
Definition
|
|
Term
| What happens if a ruminant's blood Glc drops to 20 mg/dl? |
|
Definition
| Can be tolerated for a few hours w/ no major consequence |
|
|
Term
| What are the main Glc precursors in ruminants? (%?) |
|
Definition
| Propionate (70%), aa's (20%), Lactate/Pyruvate/Glycerol |
|
|
Term
| Where do aa's as precursors to Glc come from in ruminants? |
|
Definition
|
|
Term
| How many C is propionate? |
|
Definition
|
|
Term
| Propionate is extracted by _____ (Ruminants) |
|
Definition
|
|
Term
| How does propionate enter the KC? (Ruminants) |
|
Definition
| As Succinate (carboxilation req's Vit B12, which contains Co) |
|
|
Term
| How many C is succinate? (Ruminants) |
|
Definition
|
|
Term
| How does propionate leave the Mt? (Ruminants) |
|
Definition
| As Malate to enter Gluconeogenesis |
|
|
Term
| What is the fate of propionate in ruminants? |
|
Definition
|
|
Term
| (Ruminants) Glc is released into circulation for: |
|
Definition
| Glc-dependent tissues (brain); Fetus; Milk production; Fat tissue to provide glycerol |
|
|
Term
| What does chronic Co deficiency in soil cause in cows? Where is this a problem? |
|
Definition
| Unthriftiness; Infertility; Florida & Australia |
|
|
Term
| (Ruminants) What is the fate of acetate? |
|
Definition
| Absorbed by all tissues except liver; Enters KC as Acetyl CoA for energy gain (ETC) = major energy supplier; Enters Lipogenesis as Acetyl CoA in mammary gland & fat tissue |
|
|
Term
|
Definition
|
|
Term
| (Ruminants) Acetate --> _____ |
|
Definition
| ATP (primarily) & Lipogenesis (secondarily) |
|
|
Term
| What is the major VFA from fermentation? |
|
Definition
|
|
Term
|
Definition
|
|
Term
| (Ruminants) What is the fate of Butyrate? |
|
Definition
| Partly converted in rumen epithelium & after liver uptake to KBs (irreversible) |
|
|
Term
| (Ruminants) Butyrate --> _____ |
|
Definition
|
|
Term
| What are KBs utilized for in ruminants? |
|
Definition
| Utilized in peripheral tissues for energy gain after entering KC as Acetyl CoA; Contribute to lipogenesis via Acetyl CoA in fat tissues & mammary gland |
|
|
Term
| What can cause metabolic disorders? |
|
Definition
| Endocrine disorders; Nutritional deficiencies; Genetic defects in enzymes or transport proteins |
|
|
Term
| Give examples of endocrine disorders that can cause metabolic disorders. |
|
Definition
| Diabetes Mellitus; Cushing's; Thyroids |
|
|
Term
| Give examples of nutritional deficiencies that can cause metabolic disorders. |
|
Definition
| Minerals, Trace elements, Vitamins, Lack of fuels, Lack of essential aa's; Fasting/Starvation |
|
|
Term
| Give examples of genetic disorders that cause metabolic disorders. |
|
Definition
| Glycogen storage dz's; PSSM |
|
|
Term
|
Definition
| Polysaccharide Storage Myopathy |
|
|
Term
|
Definition
|
|
Term
| What are some CS of PSSM? |
|
Definition
| Energy deficiency in mm., Hepatomegaly, Cardiomegaly, Hypoglycemia, Lactic Acidosis, Exertional Rhabdomyolysis (m. necrosis) |
|
|
Term
| What are the various forms of PSSM? |
|
Definition
| Glycogen is formed, but can't be broken down b/o enzyme defect; Abnormal glycogen type formed & stored, but can't be mobilized; Too much glycogen formed & released too fast |
|
|
Term
| What would cause glycogen to be formed but not broken down? Not to be released? |
|
Definition
| Enzyme defect (debranching enzyme); Hepatic G6Phosphatase deficiency |
|
|
Term
| Where can an abnormal glycogen type be formed & stored (& not mobilized)? |
|
Definition
|
|
Term
| What can cause too much glycogen to be formed & released too fast? |
|
Definition
| Hypersensitivity to Insulin |
|
|
Term
| What is essential to maintain basal metabolism? |
|
Definition
|
|
Term
| What must be kept constant to supply vital tissues? |
|
Definition
|
|
Term
| What are some problems w/ energy supply/Glc levels? |
|
Definition
| Irregular food intake/absorption; Gut not a nutrient storage organ; Basic energy needs constant |
|
|
Term
| What is the solution for the need for constant energy supply/Glc levels? |
|
Definition
| Whole body metabolism is dynamic & constantly switches between 2 (3) major stages |
|
|
Term
| What are the 2 (3) major stages of metabolism? |
|
Definition
| Absorptive Phase; Post-Absorptive Phase; (Fasting) |
|
|
Term
| Absorptive Phase = _____ --> _____ |
|
Definition
| Excess Energy --> Storage |
|
|
Term
| Post-Absorptive Phase = _____ --> _____ |
|
Definition
| Low energy --> Mobilization |
|
|
Term
|
Definition
| Survival; Continued mobilization |
|
|
Term
| Absorptive Phase, Post-Absorptive Phase, (& Fasting) contribute to __________. |
|
Definition
|
|
Term
| Fuel homeostasis is determined largely by ______. |
|
Definition
| Availability of blood Glc |
|
|
Term
| The _____ of fuels, esp. _____, stimulate the release of metabolic regulators (=_____), which control the flow or direction of _____. |
|
Definition
| Availability/Unavailability; Glc; Hormones; Metabolic p'ways |
|
|
Term
| What is included in a mixed meal? |
|
Definition
|
|
Term
| What is another name for the Absorptive Phase? |
|
Definition
|
|
Term
| How long is the time of active digestion & absorption of fuels? |
|
Definition
|
|
Term
| During the absorptive phase, blood levels of _____ increase. (mol's) |
|
Definition
|
|
Term
| During the absorptive phase, _____ stimulates the pancreas to release _____ & inhibits release of _____. |
|
Definition
| Hyperglycemia; Insulin; Glucagon |
|
|
Term
| What is the insulin/glucose ratio in the absorptive phase? |
|
Definition
|
|
Term
| Hyperglycemia stimulates _____ to release insulin. |
|
Definition
|
|
Term
| To what tissues does insulin make Glc available? What is the consequence of this? |
|
Definition
| All tissues; All tissues take up & utilize Glc for energy (preferred fuel) |
|
|
Term
| What p'ways does insulin stimulate in the liver? Describe. |
|
Definition
| Glycogenesis (storage of excess Glc); aa uptake, temporary storage, PP synthesis; Lipogenesis out of excess Glc & aa's & release of VLDLs |
|
|
Term
| What p'ways does insulin stimulate in mm? Describe. |
|
Definition
| Glycogenesis; aa uptake, temporary protein pool, synthesis of m. proteins |
|
|
Term
| What p'ways does insulin stimulate in fat tissue? Describe. |
|
Definition
| Endothelial LPL: FAs/Glycerol are extracted from chylomicrons & VLDLs for fat storage; Lipogenesis |
|
|
Term
| Where does insulin stimulate LPLs? |
|
Definition
|
|
Term
| In the absorptive phase, what happens to Glc (preferred fuel)? |
|
Definition
| Oxidized in all tissues for energy |
|
|
Term
| In the absorptive phase, what happens to excess nutrients? |
|
Definition
| Stored as Glycogen, Protein Pool, Fat |
|
|
Term
| What is absorbed in a carnivorous diet? |
|
Definition
| aa's & chylomicrons (very little Glc) |
|
|
Term
| In a carnivorous diet, what do aa's stimulate? |
|
Definition
| Insulin release --> stimulates uptake of aa's into cells |
|
|
Term
| In a carnivorous diet, what does hypoglycemia stimulate? |
|
Definition
| Glucagon release --> stimulates gluconeogenesis using the absorbed aa's as precursors |
|
|
Term
| Compared to herbivores/omnivores, what are the Glc demands of carnivores? |
|
Definition
|
|
Term
| What is completed during the post-absorptive phase? |
|
Definition
| Digestion & Absorption of fuels |
|
|
Term
| During the post-absorptive phase, what happens to blood levels of Glc, aa, & chylomicrons? |
|
Definition
| Decline as these fuels are taken up by tissues |
|
|
Term
| During post-absorptive phase, blood Glc levels slide toward _____. |
|
Definition
|
|
Term
| During post-absorptive phase, what does hypoglycemia stimulate? |
|
Definition
| Pancreas to release Glucagon/inhibit release of insulin; Adrenal gland to release Cortisol & Epi |
|
|
Term
| What is the insulin/glucose ratio in the post-absorptive phase? |
|
Definition
|
|
Term
| During post-absorptive phase, ______ maintain basic blood Glc levels via _____ & _____. |
|
Definition
| Glucagon, Cortisol, & Epi; Glycogenolysis (Glucagon & Epi) & Gluconeogenesis (Glucagon & Cortisol) |
|
|
Term
| During post-absorptive phase, what does lack of insulin do? |
|
Definition
| Makes sure remaining Glc is only available to Glc-dep tissues (NS, RBCs, etc) |
|
|
Term
| During post-absorptive phase, what do Glc-indep tissues use for energy gain? Provided by action of what hormone(s)? |
|
Definition
|
|
Term
| During post-absorptive phase, lack of insulin & presence of G/C/E favor what p'ways in fat tissue? Describe. |
|
Definition
| Responds to E/C/G & lack of I; Lipolysis via HSL w/ release of FAs as NEFAs & Glycerol |
|
|
Term
|
Definition
|
|
Term
| What is the effect of insulin on HSL? |
|
Definition
| HSL actively inhibited by insulin; Lack of insulin --> HSL activation |
|
|
Term
| During post-absorptive phase, lack of insulin & presence of G/C/E favor what p'ways in liver? What is the response to? |
|
Definition
| Responds to G/C/E; Glycogenolysis; Gluconeogenesis; FFA uptake from NEFAs |
|
|
Term
| Describe Glycogenolysis in the liver during the post-absorptive phase. |
|
Definition
| Glycogenolysis --> G6P w/ Glycolysis being inhibited by G --> Glc accumulates --> diffuses out of hepatocytes as free Glc (G & E) |
|
|
Term
| Describe Gluconeogenesis in the liver during the post-absorptive phase. |
|
Definition
| Gluconeogenesis from aa's & Glycerol (G & C) |
|
|
Term
| Describe FFA uptake from NEFAs in the liver during the post-absorptive phase. |
|
Definition
| FFA uptake from NEFAs --> for energy gain & some release of KBs & VLDLs |
|
|
Term
| During post-absorptive phase, lack of insulin & presence of G/C/E favor what p'ways in muslce? |
|
Definition
| Responds to C & E; Glycogenolysis for energy gain (no release of Glc); FFAs uptake from NEFAs & VLDLs & KBs for energy gain |
|
|
Term
| What tissues use Glc in the post-absorptive phase? |
|
Definition
| Reserved for Glc-dep tissues |
|
|
Term
| What happens to stored nutrients in the post-absorptive phase? |
|
Definition
| Mobilized & most tissues utilize FFAs |
|
|
Term
| During the post-absorptive phase, what do metabolic changes induce? |
|
Definition
| Hunger --> Next meal --> Absorptive Phase |
|
|
Term
|
Definition
| State of negative energy balance lasting more than a few days/weeks |
|
|
Term
| During fasting/starvation, what phase continues? |
|
Definition
|
|
Term
| During fasting/starvation, what happens to glycogen stores & how long does it take? |
|
Definition
| Depleted w/i a few hrs (6-8 h) |
|
|
Term
| What is the top priority during fasting/starvation? What does it d/o? |
|
Definition
| Maintenance of basic blood Glc levels, w/ dependency on Gluconeogenesis from aa's (Proteolysis) & Glycerol (Lipolysis) |
|
|
Term
| What is the function of lipolysis during fasting/starvation? |
|
Definition
| Provides fuel for all Glc-indep tissues |
|
|
Term
| During fasting/starvation, what is the hormone state? |
|
Definition
| Longstanding dominance of G/C/E, while I is low |
|
|
Term
| During fasting/starvation, what is used for Proteolysis? |
|
Definition
| aa's from temporary pool, then structural & functional aa's (mm. & other organs) |
|
|
Term
| During fasting/starvation, what happens in muscle & other tissues? What is the purpose of this? |
|
Definition
| Proteolysis increases to provide aa's for Gluconeogenesis |
|
|
Term
| During fasting/starvation, what happens to fat? |
|
Definition
| Lipolysis increases to provide NEFAs for E & Glycerol for Gluconeogenesis; Release of NEFAs soon exceeds body's E demands, but continues b/c hypoglycemia forces hormonal situation which accelerates HSL action |
|
|
Term
| What are the effects of HSL on hormones? |
|
Definition
| Decrease insulin; Increase C/E/G |
|
|
Term
| During fasting/starvation, what happens to the liver? |
|
Definition
| Takes up many more NEFAs ("fat sponge") than needs for E; Many FFAs repackaged & exported as VLDL, more VLDLs circulate than can be used by peripheral tissues, Hyperlipidemia (horses); Liver cells eventually run out of lipotropic factors to produce VLDLs & FFA/TG accumulate, Hepatic Lipidosis (cats, cows, horses); More KBs produced & released than can be utilized by peripheral tissues, Ketoacidosis & Ketonuria |
|
|
Term
| What is another name for Hyperlipidemia? |
|
Definition
|
|
Term
| In what animals is Hyperlipidemia a problem? |
|
Definition
|
|
Term
| What are CS of Hyperlipidemia? |
|
Definition
| Depression, Lethargy, Lipemic Plasma |
|
|
Term
| During ketoacidosis, where can acetone be smelled? |
|
Definition
|
|
Term
| What are the consequences of fasting/starvation? |
|
Definition
| m. & organ wasting/malfunctions; hepatic lipidosis leading to hepatic damage; metabolic ketoacidosis |
|
|
Term
| What is the cause of Ketosis/Hepatic Lipidosis? |
|
Definition
| Lack or unavailability of carbs (Hypoglycemia) |
|
|
Term
| When is Ketosis/Hepatic Lipidosis typically seen? |
|
Definition
| Fasting/Starvation/Anorexia in cats; Excessively high Glc demands (Pregnancy) in ponies & sm rum's/(Peak Lactation) in cows; Hormonal imbalances which lead to excessive lipolysis/proteolysis (Diabetes Mellitus); Dietary imbalances (High protein/Low carbs) |
|
|
Term
| How long does it take for an anorexic cat to enter hepatic lipidosis? |
|
Definition
|
|
Term
| When is ketosis/hepatic lipidosis primarily seen? |
|
Definition
|
|
Term
| What is the Tx for hepatic lipidosis/ketosis? (Excl. cats) |
|
Definition
| IV Glc infusion, insulin, buffer, electrolytes |
|
|
Term
| What is the Tx for hepatic lipidosis/ketosis in cats? Why isn't Glc given directly? |
|
Definition
| Give aa's so cat can synthesize own Glc; Cats convert carbs to fat & make situation worse |
|
|
Term
| What is the #1 reason for liver failure in cats in the US? |
|
Definition
| Ketosis/Hepatic Lipidosis |
|
|
Term
| What is the term for ketosis/hepatic lipidemia caused by pregnancy? |
|
Definition
|
|
Term
| When are CS of ketosis/hepatic lipidosis seen? |
|
Definition
|
|
Term
| Many metabolic pways are _____-specific. |
|
Definition
|
|
Term
| Can other organs compensate for the metabolic pways disrupted in liver failure? |
|
Definition
|
|
Term
| What types of metabolism is the liver involved in? |
|
Definition
|
|
Term
| What are some liver functions aside from metabolism? |
|
Definition
| Blood Reservoir (EPO); Defense (Kupffer cells); Vit/mineral/trace element storage; Detox/excretion of drugs, hormones, bilirubin, urea |
|
|
Term
|
Definition
|
|
Term
| From what does bilirubin originate? |
|
Definition
|
|
Term
| What happens to bilirubin when it leaves RES cells? |
|
Definition
| Binds to Albumin = Plasma form/U-BILI/Indirect BILI |
|
|
Term
|
Definition
|
|
Term
|
Definition
| Taken up by liver cells (carrier mediated) & conjugated w/ Glucuronic acid = C-BILI/Direct BILI |
|
|
Term
|
Definition
|
|
Term
| What is the rate-limiting step of bile pigment secretion in horses? |
|
Definition
| U-BILI taken up into liver cells (carrier mediated) |
|
|
Term
| Describe the capacity of carriers to mediate the uptake of U-BILI into liver cells. |
|
Definition
| High capacity except in horses |
|
|
Term
| What is the purpose of conjugating BILI? |
|
Definition
| Makes water-soluble for excretion |
|
|
Term
| What happens to C-BILI when it is formed? |
|
Definition
| Secreted into bile ducts; Some regurgitated into circulation |
|
|
Term
| What is the rate-limiting step of bile pigment secretion in all spp. except horses? |
|
Definition
| Secretion of C-BILI into bile ducts |
|
|
Term
| What happens to C-BILI in the intestines? |
|
Definition
| Converted via urobilinogen/stercobilinogen to Urobilin/Stercobilin (dark color of feces) |
|
|
Term
| What type of bilirubin is normally present in plasma? |
|
Definition
| Both U-BILI & C-BILI (50/50 in most spp; more U in horses) |
|
|
Term
| What is jaundice/icterus? |
|
Definition
| Yellow pigmentation of skin/mucosa/body fluids caused by deposition of bilirubin |
|
|
Term
| Why is jaundice dangerous in neonates? |
|
Definition
| Blood-brain barrier not fully formed; can enter brain |
|
|
Term
| What are the 3 types of jaundice? |
|
Definition
| Pre-Heptatic; Hepatic; Post-Hepatic |
|
|
Term
| What causes pre-hepatic jaundice? |
|
Definition
| Excessive breakdown of Hb (Hemolytic disorders, Massive internal bleedings; Signs of anemia) |
|
|
Term
| What is also seen in pre-hepatic jaundice? |
|
Definition
|
|
Term
| What happens to bilirubin production in pre-hepatic jaundice? |
|
Definition
| U-BILI production increases beyond capacity of liver for uptake & conjugation |
|
|
Term
| In pre-hepatic jaundice, what is elevated initially? Later? |
|
Definition
| U-BILI; Both forms increase as secretion of C-BILI becomes saturated |
|
|
Term
| What type of bilirubin dominates in pre-hepatic jaundice? |
|
Definition
|
|
Term
| What causes hepatic jaundice? Give examples. |
|
Definition
| Damage to liver cells (inflammation, lipidosis, necrosis) |
|
|
Term
| In hepatic jaundice, what happens to secretion of bilirubin? |
|
Definition
| C-BILI secretion initially more impaired than U-BILI uptake & conjugation |
|
|
Term
| In hepatic jaundice, what is elevated initially? Later? |
|
Definition
| C-BILI in most cases (b/o regurgitation); U-BILI also increases as uptake becomes impaired |
|
|
Term
| What causes post-hepatic jaundice? |
|
Definition
| Obstruction of bile ducts (stones, tumors, intrahepatic cholestasis) |
|
|
Term
| What is the most variable type of jaundice wrt dominance of C-BILI/U-BILI? |
|
Definition
| Hepatic (Typically C>U; not always) |
|
|
Term
| What type of bilirubin dominates in post-hepatic jaundice? |
|
Definition
|
|
Term
| What happens to C-BILI in post-hepatic jaundice? |
|
Definition
| Regurgitated into circulation |
|
|
Term
| In post-hepatic jaundice, increased ______ can ultimately cause _____ injury. |
|
Definition
| Intrahepatic pressure; Hepatocellular |
|
|
Term
| In post-hepatic jaundice, what is elevated initially? Later? |
|
Definition
| C-BILI very dominant initially; Later U-BILI can also increase (cell damage) |
|
|
Term
| What types of bilirubin can be tested? |
|
Definition
| Total & C (U is indirect) |
|
|
Term
| What byproduct of metabolism is important in thermoregulation? |
|
Definition
|
|
Term
|
Definition
| Rise in the hypothalamic set point |
|
|
Term
| What is the normal body temperature in humans? |
|
Definition
|
|
Term
| What is the normal body temperature in birds? |
|
Definition
|
|
Term
| Where is the temperature regulating center? What is it? |
|
Definition
| Hypothalamus; Thermostat w/ fixed set point (core temperature) |
|
|
Term
| What informs the hypothalamus of body temperature? What does this initiate? |
|
Definition
| Superficial & Deep temperature Rs; Heat loss or conservation mechanisms |
|
|
Term
| What are heat losing mechanisms? |
|
Definition
| Vasodilation, Sweating, Panting, Behavior, Decreased Basal Rate, Decreased Food intake |
|
|
Term
| What is the most important heat losing mechanism? |
|
Definition
|
|
Term
| What is the most important heat conserving mechanism? |
|
Definition
|
|
Term
| What are heat conserving mechanisms? |
|
Definition
| Vasoconstriction, Piloerection (insulation), Increased metabolic rate, Shivering, Behavior, Increased food intake |
|
|
Term
| What are the 2 main causes of fever? |
|
Definition
| Pyrogens & Compression of hypothalamus |
|
|
Term
| What can compress the hypothalamus leading to fever? |
|
Definition
|
|
Term
| What are some examples of pyrogens? |
|
Definition
| Bacterial toxins, protein breakdown products, Cytokines (IL1,6,8,TNF) |
|
|
Term
| How do pyrogens cause fever? |
|
Definition
| Reset hypothalamic thermostat to higher value (induce formation of PGE2) |
|
|
Term
| What type of drugs are anti-pyretic? |
|
Definition
| Those which inhibit PG synthesis, ex: NSAIDs |
|
|
Term
| How is fever initially a helpful response? |
|
Definition
| Increases metabolism & circulation, activates defense system, suppresses pathogen replication |
|
|
Term
| What are characteristics of fever? |
|
Definition
| Chill Phase & Crisis Phase |
|
|
Term
| What is the Chill Phase of fever? |
|
Definition
| Body attempts to reach new set pt by shivering, piloerection, vasoconstriction, behavior etc. (Heat-conserving mechanisms) |
|
|
Term
| What is the Crisis Phase of fever? |
|
Definition
| After removal of fever inducing factor, set pt returns to normal, Heat-losing mechanisms are initiated |
|
|
Term
|
Definition
| Severe vasoconstriction; Freezing of superficial areas w/ crystal formation; Permanent tissue damage |
|
|
Term
|
Definition
| Heat loss>Heat production |
|
|
Term
| wrt Hypothermia, when do heat regulating mechanisms become impaired? |
|
Definition
|
|
Term
| wrt Hypothermia, when does cardiac arrest occur? |
|
Definition
|
|
Term
| What is another term for Hyperthermia? |
|
Definition
|
|
Term
| What is hyperthermia? Give some examples. |
|
Definition
| Heat loss cant keep up w/ heat generation; Heavy exercise in hot-humid conditions, Enclosure in hot-humid rooms or cars |
|
|
Term
| What happens to temperature in hyperthermia? |
|
Definition
| Body temp rises; Heavy sweating/panting, but insufficient cooling effect b/o high ambient temp & humidity |
|
|
Term
| What happens to fluids in hyperthermia? |
|
Definition
| Fluid loss; Dehydration; Initial BP drop; Sympathetic response; Vasoconstriction; Disables further heat loss |
|
|
Term
| What happens when core temp increases above 41.5-42.5C? |
|
Definition
| Impairment of cellular functions; Endothelial damage via hypoxia & protein denaturation; Plasma leakage & hemorrhages; Dizziness, Nausea, Coma, Death (CNS, Kidneys, Liver, GI, mm.) |
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