9. Biochemistry p163-171

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Lipoprotein functions: p. 163
Chylomicrons deliver dietary _____ to ________ and dietary ______ to ______.: Triglycerides, peripheral tissues; Cholesterol, liver
Which cells secrete chylomicrons?: Intestinal epithelial cells
Secretion is mediated by apolipoprotein _______.: B-48
True/False: VLDL delivers hepatic triglycerides to peripheral tissues.: TRUE
Where is VLDL secreted from?: Liver
LDL delivers hepatic cholesterol to _______.: Peripheral tissues
LDL is taken up by target cells via what process?: Receptor-mediated endocytosis
HDL mediates transport of cholesterol from where to where?: Periphery to liver (reverse cholesterol transport)
HDL acts as a repository for ______ and _______.: apoC and apoE
HDL is secreted from which 2 places?: Liver and intestine
Familial dyslipidemias: p. 163
Type I (hyperchylomicronemia) has elevated blood levels of ______.: Triglycerides
Type IIa (hypercholesterolemia) has increased levels of what?: LDL
What is the pathophysiology of type Iia?: Decreased number of LDL receptors
Type IIb (combined hyperlipidemia) has increased levels of ____ and _____.: LDL, VLDL
Type III (dysbetalipoproteinemia) has altered apolipoprotein __, and increased ____ and _____.: E, IDL, VLDL
Type IV (hypertriglyceridemia) is caused by hepatic overproduction of what?: VLDL
True/False: Type V (mixed hypertriglyericdemia) has only increased VLDL: False; Increased VLDL and chylomicrons
Metabolism sites: p. 163
Identify the site of metabolism (Mitochondria, Cytoplasm, or Both)
Fatty acid oxidation (Beta-oxidation): Mitochondria
Glycolysis: Cytoplasm
Gluconeogenesis: Both
Fatty acid synthesis: Cytoplasm
Urea cycle: Both
Acetyl-CoA production: Mitochondria
Heme synthesis: Both
HMP Shunt: Cytoplasm
Protein synthesis (RER): Cytoplasm
Steroid synthesis (SER): Cytoplasm
Aminolevulinate (ALA) synthesis: p. 165
ALA synthesis is the rate-limiting step for the produciton of what?: Heme
ALA is found in the ______: Mitochondria
Heme synthesis: p. 165
Heme synthesis occurs in the ______ and ________.: Liver, bone marrow
Underproduction of heme causes ___________ ___________ _________.: Microcytic hypochromatic anemia
Accumulation of intermediates causes what?: Porphyria
Porphyrias: p. 165
This type of porphyria is marked by a deficiency in uroporphyrinogen I synthetase: Acute intermittent porphyria
How does lead affect iron incorporation into heme?: It prevents it
This is the most common type of porphyria; a deficiency in uroporphynogen decarboxylase): Porphyria cutanea tarda
Heme catabolism: p. 165
True/False: The progression of heme catabolism is heme --> biliverdin --> bilirubin: TRUE
Bilirubin is (Toxic/Non-toxic) to CNS and transported by _________.: Toxic, albumin
In the liver, heme is conjugated with __________.: Glucoronate
True/False: Urobilinogen is an intestinal intermediate that is never found in the blood and urine.: False: a small amount is reabsorbed into blood and excreted in urine.
Hemoglobin: p. 165
Hemoglobin is composed of many polypeptide subunits?: 4 (2 alpha, 2 beta)
Carbon monoxide has a 200x (higher/lower) affinity for hemoglobin than does oxygen: Higher
T (taut) form of hemoglobin has a (high/low) affinity for oxygen: Low
R (relaxed) form of hemoglobin has a (high/low) affinity for oxygen: High
True/False: Myoglobin, like hemoglobin, has a sigmoid-shaped O2 binding curve.: FALSE
Hemoglobin structure regulation: p. 165
Increased Cl, H, CO2, DPG, and temperature favor shift over curve to (left/right).: Right (unloads more O2)
True/False: Shift to right is due to preference for T form over R form.: TRUE
Methemoglobinemia: p. 165
True/False: Methemoglobin is an oxidized form of hemoglobin that binds O2 more readily.: False: it binds O2 less readily
CO2 transport in blood
CO2 binds to (heme/amino acids in globin chain).: Amino acids in globin chain
CO2 binding favors which form of hemoglobin? And what sort of shift does it cause?: T. Right shift.
Vitamins: fat soluble: p. 166
What are the fat soluble vitamins?: A,D,E,K
The absorption of fat soluble vitamins depends on what two organs?: small intestine (ileum) and pancreas
Is toxicity more common for fat or water soluble vitamins?: fat soluble becauase the vitamins accumulate in the fat
What can cause fat-soluble vitamin deficiencies besides just general lack of intake?: malabsorption syndromes and mineral oil intake
Vitamins: water soluble: p. 166
What are the water soluble vitamins?: B1, 2, 3, 5, 6, 12, C, Biotin, Folate
What do B complex deficiencies cause?: dermatitis, glossitis, and diarrhea
Vitamin A (retinol): p. 166
What is the function of vitamin A?: constituent of visual pigments
Match up the appropriate vitamin with these alternates names? A.thiamine, B.riboflavin, C.niacin, D.retinol,: C2
What does a deficiency of vitamin A cause?: night blindness and dry skin
Vitamin B1 (thiamine): p. 166
What does a deficiency of vitamin B1 cause?: Ber1Ber1 and Wernicke-Korsakoff syndrome
What is the function of vitamin B1?: Cofactor for oxidative decarboxylation of alpha-keto acids and a transketolase in the HMP shunt.
Beriberi is characterized by what 3 symptoms?: polyneuritis, cardiac pathology, and edema
Vitamin B2 (riboflavin): p. 167
What does a deficiency of vitamin B2 cause?: angular stomatitis, cheilosis, corneal vascularization
What is the function of vitamin B2?: cofactor in oxidation and reduction
Vitamin B3 (niacin): p. 167
What is vitamin B3 a constituent of?: NAD+, NADP+
What does a deficiency of vitamin B3 cause?: Pellagra
What are the symptoms of pellagra?: Diarrhea, Dermatitis, Dementia
Vitamin B5 (pantothenate): p. 167
What is vitamin B5 a constituent of?: CoA
A deficiency in vitamin B5 causes what 4 problems?: dermatitis, enteritis, alopecia, adrenal insufficiency
Vitamin B6 (pyridoxine): p. 167
When vitamin B6 is converted to ___, it is a cofactor in what three processes?: pyridoxal phosphate; cofactor in transamination, decarboxylation, and trans-sulfuration
What may induce a deficiency in vitamin B6?: INH and oral contraceptives
Biotin: p. 167
Biotin is a cofactor in which 3 carboxylations?: pyruvate to oxaloacetate, acetyl-CoA to malonyl CoA, and proprionyl-CoA to methylmalonylCoA
The use of __ and ingestion of __ cause a deficiency in biotin?: antibiotics; raw eggs
Folic acid: p. 167
What is the most common vitamin deficiency in the US?: folic acid
Neurologic symptoms with anemia are seen in folic acid or B12 deficiency?: B12
What is folic acid important in the synthesis of?: Nitrogenous bases in DNA and RNA
What two drugs are PABA analogues (the precursor of folic acid in bacteria)?: sulfa drugs and dapsone
Vitamin B12 (cobalamin): p. 168
Vitamin B12 is involved in which two conversions?: Homocysteine to Methionine and Metholmalonyl CoA to SuccinylCoA
Where is vitamin B12 stored: liver
What are the 3 main causes of vitamin B12 defiiciency?: malabsorption, lack of intrinsic factor, and absence of terminal ileum
What test is used to determine a deficiency of vitamin B12: Schilling
Vitamin C (ascorbic acid): p. 169
Deficiency of Vit C causes what?: Scurvy
Vit C is necessary for ________ of proline and lysine in ________ synthesis: hydroxylation / collagen
Vit C also facilitates absorption of what?: Iron - by keeping iron in Fe2+ reduced state
Vit C is necessary as a cofactor for what?: Dopamine --> NE
What are the clinical findings of scurvy?: Swollen Gums, bruising, anemia, poor wound healing
Vitamin D: p. 169
D2, also called _______ is consumed from what?: ergocalciferol, comsumed in milk
Cholecalciferol, also called ____ is formed where?: D3, formed in sun-exposed skin
25-OH D3 is what form of Vit D: Storage form
1,25 (OH)2D3 is what form of Vit D: Active form
Deficiency of Vit D in children causes? In adults?: Children - Rickets // Adults - Osteomalacia. Also can cause hypocalcemic tetany
Vit D functions to: Increase intestinal absorption of calcium and phosphate
Too Much Vitamin D has three clinical effects. What are they?: Hypercalcemia, loss of appetite, stupor.
The 6 causes of hypercalcemia are:: Vit D. Intoxication / Malignancy / Hyperparathyroidism / Milk-Alkali syndrome / Sarcoidosis / Paget's disease of bone
Excess Vit D is seen in what disease state?: Sarcoidosis - where epithelial macrophages convert vit D into its active form
Vitamin E: p. 169
Deficiency in Vit E causes?: Increased fragility of erythrocytes (E is for erythrocytes)
Vit E functions as an ______ to protect _______: Antioxidant, to protect erythrocytes from hemolysis
Vitamin K: p. 169
T/F - Vitamin K deficiency causes neonatal thrombi and pulmonary emboli.: False - Vit K deficiency causes - neonatal hemorrhage
How does Vit K effect the PT, aPTT and Bleeding time?: Increased PT and aPTT but normal bleeding time.
What coagulation factors require Vitamin K?: Factors II, VII, IX, X and protein C and S. (remember 1972).
How does warfarin work?: It is a vitamin K antagonist.
What does Vit K catalyze?: The gamma-carboxylation of glutamic acid residues on various proteins concerned with blood clotting.
Where is Vit K synthesized?: Vit K is synthesized by the normal intestinal flora.
Ethanol Metabolism: p. 169
What are the two enzymes required to convert Ethanol --> acetaldehyde --> acetate?: Alcohol dehydrogenase for the first reaction, and acetaldehyde dehydrogenase for the second.
What is the limiting reagent in the above reaction?: NAD+ is the limiting reagent for both reactions
How does Disulfiram work?: Disulfiram (antabuse) - inhibits acetaldehyde dehydrogenase (acetaldehyde accumulates, contributing to hangover symptoms)
When I go out drinking with the class of 2006, why is PBL so painful the next morning?: Because acetaldehyde accumulates in my system, and after 2 years, PBL is always painful.
Ethanol Hypoglycemia: p. 170
How does ethanol metabolism lead to hypoglycemia?: Ethanol metabolism increases NADH/NAD+ ratio in the liver, causing diversion of pyruvate to lactate and OAA to malate, thereby inhibiting gluconeogenesis and leading to hypoglycemia.
What is hepatocellular steatosis, and how does it occur?: Hepatocellular steatosis = hepatic fatty changeÂ… It occurs because of the above pathway resulting in an increase in NADH/NAD+ ratio, which causes a shunting away from glycolysis and toward fatty acid synthesis.
Kwashiorkor vs. marasmus: p. 170
What is kwashiorkor?: Protein malnutrition resulting in skin lesions, edema, liver malfunction (fatty change).
What is marasmus?: protein - calorie malnutrition resulting in tissue wasting.
The clinical picture of a small child with a swollen belly is characteristic of kwashiorkor or marasmus?: Kwashiorkor
Kawashiorkor results from a protein-deficient M.E.A.L. What does M.E.A.L. stand for?: Malabsorption, Edema, Anemia, Liver (fatty)
Summary of pathways: p.171
Glucose is first converted to what in the cell?: Glucose-6-phosphate
What are the three products that glucose-6-phosphate is converted to in the cell?: Glucose-1-P (to glycogen pathway) // Fructose-6-P (To TCA) // 6-phosphogluconolactone (to Ribose-5 phosphate pathway)
What are the steps of the TCA?: Acetyl-CoA --> Citrate --> Isocitrate --> alpha-ketoglutarate --> Succinyl-CoA --> Succinate --> Fumarate --> Malate --> Oxaloacetate
What are the steps of the Urea Cycle?: Aspartate --> Arginosuccinate --> Arginine --> Ornithine --> Citrulline --> Arginosuccinate
Odd chain fatty acids enter the TCA through what series of molecules?: Odd chain FA --> Propionyl-CoA --> Methylmalonyl-CoA --> Succinyl-CoAÂ… into TCA
Acetyl Co-A, aside from entering the TCA, can be converted into what three molecules?: Mevalonic acid, Acetoacetyl-CoA, malonyl-CoA
Beta - hydroxybutyrate is formed from Acetyl-CoA through what precursors?: Acetyl-CoA --> Acetoacetyl-CoA --> Acetoacetate --> Beta-hydroxybutyrate
Cholesterol is formed from acetyl co-A through what precursors?: Acetyl-CoA --> Mevalonic Acid --> Isoprene --> Squalene --> Lanosterol --> Cholesterol
The conversion of Arginine to Ornithine creates as a byproduct, what?: H20 --> Urea
NH4 + CO2, leads to _______, and enters the Urea cycle where?: Leads to Carbamoyl Phosphate, enters at the conversion of ornithine --> citrulline
Write the steps of conversion of glucose to acetyl-CoA: Glucose --> Glucose -6-P --> Fructose-6-P --> fructose-1,6-bisphosphate --> glyceraldehyde-3P --> 1,3-bis-phosphoglycerate --> 3-phosphoglycerate --> 2-phosphoglycerate --> phosphoenolpyruvate --> pyruvate --> acetyl-coA

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