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154 Cards in this Set

  • Front
  • Back
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 _______.
True/False: VLDL delivers hepatic triglycerides to peripheral tissues.
Where is VLDL secreted from?
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 ______.
Type IIa (hypercholesterolemia) has increased levels of what?
What is the pathophysiology of type Iia?
Decreased number of LDL receptors
Type IIb (combined hyperlipidemia) has increased levels of ____ and _____.
Type III (dysbetalipoproteinemia) has altered apolipoprotein __, and increased ____ and _____.
Type IV (hypertriglyceridemia) is caused by hepatic overproduction of what?
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)
Fatty acid synthesis
Urea cycle
Acetyl-CoA production
Heme synthesis
HMP Shunt
Protein synthesis (RER)
Steroid synthesis (SER)
Aminolevulinate (ALA) synthesis
p. 165
ALA synthesis is the rate-limiting step for the produciton of what?
ALA is found in the ______
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?
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
Bilirubin is (Toxic/Non-toxic) to CNS and transported by _________.
Toxic, albumin
In the liver, heme is conjugated with __________.
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.
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
T (taut) form of hemoglobin has a (high/low) affinity for oxygen
R (relaxed) form of hemoglobin has a (high/low) affinity for oxygen
True/False: Myoglobin, like hemoglobin, has a sigmoid-shaped O2 binding curve.
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.
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?
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,
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?
What does a deficiency of vitamin B3 cause?
What are the symptoms of pellagra?
Diarrhea, Dermatitis, Dementia
Vitamin B5 (pantothenate)
p. 167
What is vitamin B5 a constituent of?
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
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?
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
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
Vitamin C (ascorbic acid)
p. 169
Deficiency of Vit C causes what?
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 change… 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?
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
Glucose is first converted to what in the cell?
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-CoA… 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