Biochemistry: Metabolism Flashcards

Question

Activated carrier: ATP

Answer 1

Phosphoryl groups

Answer 2

Acyl groups

Answer 3

1 carbon unit

Answer 4

CH3 groups

Answer 5

Nicotinamides (NAD+ and NADP+) and flavin (FAD+) * NAD is generally used in catabolic processes to carry reduing equivalencts away as NADH * NADPH is used to anabolic processes ( steroid and fatty acid synthesis) as a supply of reducing equivalents * product of HMP shunt * repiratory burst * Cytochrome P450 system * Glutathione reductase

Answer 6

catalyzes phosphorylation of glucose to yield G6P is the 1st step of glycolysis in most tissue * not liver or B- cells in pancreas * Lower Km ( increase affinity) * Vmax lower (decrease capacity) * Not induced by insulin * Feedback inhibited by G6P * No gene mutation associated with maturity onset diabetes

Answer 7

Phosphorylation of glucose to G6P ( glycolysis) * Liver, B-cells in pancreas * Km: higher (lower affinity) * Vm: higher ( increase capacity) * Induced by insulin * no feedback inhibition by G6P * associated with gene mutation in maturity-onset diabetes of the young

Answer 8

Cytoplasm * Glucose + 2Pi +2ADP + NAD+ --\> * 2 pyruvate + 2ATP + 2 NADH +2H₂O + 2H⁺

Answer 9

* Glucose--\> Glucose 6 phosphate * Hexokinase/ glucokinase * Glu 6P (-) hexokinase * Fru 6P (-) glucokinase * Fructose 6P--\> Fru 1, 6BP * Phosphofructokinase 1 ( rate limiting) * ATP (-) * AMP (+) * citrate (-) * Fru 2,6 BP (+)

Answer 10

* 1,3 BPG \<--\> 3 PG * Phosphoglycerate kinase * Phosphoenolpyruvate --\> pyruvate * pyruvate kinase * ATP (-) * alanine (-) * Fru 1,6 BP (+)

Answer 11

* Fructose 6 Phosphate \<--\> Fru 2,6 BP * Fed: Phosphofructokinase 2 * Fasting: Fructose bisphosphatase-2 * Fru 6P --\> Fru 1,6BP * PFK-1 * (+) PFK2 * glycolysis * Fru 1,6BP --\> Fru 6P * FBPase-1 * Gluconeogenesis * Fasting state * increased glucagon--\> incr.cAMP --\> incr. PKA --\> Incr. FBPase-2 --\> decr. PFK-2 * Less glycolysis and more gluconeogenesis * Fed state * Incr. insulin --\> decr. cAMP --\> decr. PKA --\> decr. FBPase-2 --\> incr. PFK-2 * more glycolysis * less gluconeogenesis

Answer 12

* Pyruvate + NAD⁺ + CoA --\> acetyl coA + CO2 +NADH * Co-factors * pyrophosphate (B1, thiamine, TPP) * FAD (B2, Riboflavin) * NAD (B3, Niacin) * CoA (B5, pantothenate) * Lipoic acid (inhibited by arsenic) * Activated by exercise * Increases NAD+/NADH ratio * increase ADP * Increase Ca²⁺

Answer 13

Cuases a buildup of pyruvate that gets shunted to lactate (via LDH) and alanine (via ALT) * Neurologic defects * lactic acidosis * increase serum alanine starting in infancy * Tx: increase intake of ketogenic nutrients * high fat or increase lysine, leucine

Answer 14

* Alanine * alanine aminot transferase * B6 * carries amino groups from liver to muscle * Oxaloacetate * Pyruvate carboxylase * biotine * replenish TCA cycle or used in gluconeogenesis * Acetyl CoA * Pyruvate dehydrogenase * B1, B2, B3, B5, lipoic acid * glycolysis to TCA cycle * Lactate * lactic acid dehydrogenase * B3 * anaerobic glycolysis

Answer 15

* Produces: 3 NADH, 1 FADH₂, 2CO_2,1 GTP per acetyl CoA * 10 ATP per acetyle CoA * occurs in the mitochondria * a-ketoglutarate dehydrogenase requires * B1, B2, B3, B5, lipoic acid * Citrate Is Kreb's Starting Substrate For Making Oxaloacetate * Citrate (Citrate synthase) * Isocitrate * a- ketoglutarate ( isocitrate dehydrogenase) * Succinyl CoA (a-KG dehydrogenase) * Succinate * Fumarate * Malate * Oxaloacetate

Answer 16

NADH electrons form glycolysis enter mitochondria via the malate-aspartate or G3P shuttle * Complex I: NADH--\> NAD+ * Complex II: FADH2 --\> FAD * succinate dehydrogenase * FADH2 electrons are transfered to complex II * Complex III: CoQ * Complex IV: 1/2 +2H⁺ --\> H₂O * Complex V: ADP +Pi --\> ATP

Answer 17

* 1 NADH --\> 2.5 ATP * 1 FADH₂ --\> 1.5 ATP

Answer 18

* Complex I: Rotenone * Complex III: Antimycin A * Complex IV: Cyanide, CO * Complex V: Oligomycin

Answer 19

* Electron transport inhibitors: * directly inhibit electron transport * causing decrease in proton gradient and block of ATP synthesis * ATP synthase inhibitors * directly inhibit ATP synthase causing an increase in proton gradient * No ATP is produced because electron transport stops * Uncoupling agents * increas permability of membrane * causes a decrease in proton gradient * increase in O2 consumption * electron transport continues * produces heat * 2,4 Dinitrophenol, aspirin, thermogenin

Answer 20

* Pyruvate carboxylase * mitochrondria * Pyruvate --\> oxaloacetate * requires biotin, ATP * activated by Acetyl coA * Phosphoenolpyruvate carboxykinase * Cytosol * Oxaloacetate --\> phosphoenolpyruvate * requires GTP * Fructose 1,6, bisphosphatase * cytosol * Fruc 1,6BP --\> Fru 6P * Citrate (+) * Fru 2,6 (-) * Glucose 6 phosphatase * ER * G6P --\> glucose

Answer 21

* Occurs primarily in liver to maintain euglycemia during fasting * deficiency of key gluconeogenic enzymes cause hypoglycemia * Odd chain fatty acid yields 1 propionyl CoA during metabolism which can enter TCA, undergo gluconeogenesis and serve as glucose source

Answer 22

* Provides a source of NADPH from G6P * NADPH required for reductive reactions * glutathione reduction in RBC * Fatty acid and cholesterol biosynthesis * yields ribose for nucleotide synthesis and glycolytic intermediates * occurs in cytoplasm * No ATP used or produced * Sites * lactaing mammary glands * liver * adrenal cortex ( site of fatty acid or steroid synthesis) * RBCs

Answer 23

Irreversible * Glucose 6P --\> --\> NADPH * Glu 6P dehydrogenase * Rate limiting * requires NADP+ * Products: CO + 2NADPH +Ribulose 5P Reversible * Ribulose 5 P \<--\> Ribose 5 P * Phosphopentose isomerase, transketolase * Requires B1 * Products: RIbose 5P, G3P, F6P

Answer 24

* Activation of phagocyte NADPH oxidase (neutrophils, monocytes) * utilizes O₂ as substrate * rapid release of ROS * Phagolysosome * NADPH oxidase * Superoxide dismutase * myeloperoxidase * Glutathionine peroxidase ( requires selenium) * Glutathionine reductase (requires selenium) * G6PD

Answer 25

* Deficiency in NADPH oxidase * can use H₂O₂ generated by invading organisms and convert it to ROS * increase risk for infections by catalase (+) species * S.aureus, Aspergillus capapble of neutralizing their own H2O2 * phagocytes have no ROS for fighting infections

Answer 26

* O₂ * O₂^- (Superoxide) [_NADPH oxidase]_ * H202 _[Superoxide dismutase_] * HOCl (hypochlorite) [_Myeloperoxidase]_ __ Bacterial catalase * H2O2--\> H20 + O2 Glutathione peroxidase * H202 --\> H20 * GSH (reduced) --\> GSSG

Answer 27

* NADPH is necessary to keep glutathione reduced * Glutathione detoxifies free radicals and peroxides * decreased in NADPH in RBC= hemolytic anemia * oxidizing agents: fava beans, sulfonamides, primaquine, anti-TB drugs * infection can also precipitate hemolysis * X-linked recessive * increased malarial resistance * Heinz bodies= oxidized Hemoglobin precipitated in RBC * Bite cells: phagocytc removal of Heinz bodies by splenic macrophages

Answer 28

* defect in fructokinase * autosomal recessive * benign, asymptomatic condition * Sxs: fructose appears in urine and blood

Answer 29

* Hereditary deficiency of Aldolase B * autosomal recessive * Fructose -1-P accumulates causing decrease in available phosphate * inhibits glycogenolysis and gluconeogenesis * Sxs: present with consumption of fruit, juice, honey * hypoglycemia, jaundice, cirrhosis, vomiting * Urine dipstick will be negative * reducing sugar can be detected in urine * Tx: decrease intake of fructose and sucrose

Answer 30

* Fructose * Fru 1 P [Fructokinase] * Dihydroxyacetone-P [aldolase B] * Glyceraldehyde [aldolase B] * Glyceraldehyde 3P [Triose kinase] * Glyceraldehyde 3p --\> glycolysis

Answer 31

Hereditary deficiency of galactokinase * Galacititol accumulates if galactose is present * autosomal recessive * Sxs: galactose appears in blood and urine, infantile cateracts * May present intially as failure to track objects or develop a social smile

Answer 32

Absence of galactose-1-P uridyltransferase * Galactose 1p --\> Glucose 1 P * [Uridyltransferase] * autosomal recessive * accumulation of toxic substances * galacititol accummulates in lens of eye * Sxs: failure to thrive, jaundice, hepatosplenomegaly, infantile cateracts, intellectual disability * Tx: exclude galactose and lactose from diet * Can lead to neonatal sepsis in neonates

Answer 33

* alternative method of trapping glucose in cell is to convert it to its alcohol counterpart, sorbitol * some tissues convert sorbitol to fructose _[sorbitol dehydrogenase_] * Tissues with insufficienct enzyme can accumulate sorbitol causing osmotic damage * cataracts, retinopathy, peripheral neuropathy in chronic hyperglycemia * high levels of galataose also results in conversion to galactitol [_aldose reductase]_

Answer 34

Insufficiency lactase enzyme * Dietary lactose intolerance * lactase digests lactose into glucose and galactose * Primary: age dependant decline after childhood * Secondary: loss of brush border due to gastroenteritis (rotovirus), autoimmune disease * Congenital: rare due to defective genes * Stool: decreased pH * Breath: increase hydrogen content * intestinal biopsy reveals normal mucosa in patients with hereditary lactose intolerance * FIndings: bloating, flatulence, osmotic diarrhea * tx: avoid dairy products, lactase pills,

Answer 35

* Glucogenic: * Methionine (Met) * Valine (val) * Histidine (His) * Glucogenic/ketogenic * isoleucine (Ile) * phenylalanine (Phe) * Threonine (thr) * Tryptophan (Trp) * Ketogenic * Leucine (Leu) * Lysine (lys)

Answer 36

* Aspartic acid (Asp) * Glutamic acid (glu) * negatively charged at body pH

Answer 37

* Arginine (arg)-- most basic * Lysine (lys) * Histidine (his)-- no charge at body pH * Arg and His are required during periods of growth * Arg and lys are increased in histones which bind negatively charged DNA

Answer 38

amino acid catabolism * Forms pyruvate, acetyl-coA for metabolic fuel * Ordinarily, Careless Crappers Are Also Frivolous about Urination * Ornithine + Carbamoyl phosphate * Citrulline [_ornithine transcarbamylase_] * + Aspartate--\> Argininosuccinate [_Argininosusccinate synthetase]_ * Fumarate + Arginine [Argininosuccinase] * Urea + Ornithine [Arginase] * Carbamoyl phosphate synthetase * makes carbamoyl phosphate * requires N-acetylglutamate

Answer 39

Muscle * Amino acids (NH₃) --\> a- ketoacids * A-ketoglutarate--\> Glutamate (NH3) * Glutamate (NH3)--\> a-ketoglutarate * Pyruvate--\> alanine (NH3) Liver * alanine (NH3) --\> pyruvate * a-ketoglutarate --\> glutamate (NH3) --\> urea (NH3) * Pyruvate --\> glucose (transported to muscle) Muscle * Glucose --\> pyruvate--\> lactate (Cori cycle)

Answer 40

Results in excess NH4⁺ * depletes a-ketoglutarate * inhibits TCA cycle * Tx: limit protein in diet * Benzoate or pehnylbutyrate can be given to decrease ammonia levels * Lactulose can acidify GI tract and trap NH4+ for excretion * Sxs: tremor (asterixis, slurring of speech, somnolence, vomiting, cerebral edema, blurring of vision)

Answer 41

* Required co-factor for carbamoyl phosphate synthetase I in Urea cycle * Increased ornithine in urea cyce suggests hereditary deficiency

Answer 42

* Most common urea cycle disorder * x-linked * inability to eliminated ammonia * excess carbamoyl phosphate is converted to orotic acid * Findings: increased orotic acid in blood and urine, decreased BUN, sx of hyperammonia * no megaloblastic anemia (vs orotic aciduria)

Answer 43

* Thyrosine (BH4) * Thyroxine * --\> Dopa (BH4) * Melanine * --\> Dopamine (B6) * --\> NE (vitamin C) * --\> Epi (SAM)

Answer 44

* Niacin (B6) * NAD/NADP+ * Serotonin (BH4, B6) * Melatonin

Answer 45

* Histamine (B6)

Answer 46

* Porphyrin (B6) * Heme

Answer 47

* GABA (B6) * Glutathionine

Answer 48

* Creatinine * Urea * Nitric Oxide (BH4)

Answer 49

Decreased phenylalanine hydroxylase or tetrahydrobiopterin (BH4) * Increase in phenylalanine lees to excess phenylketones in urine * phenylketones ( phenylacetate, phenylactate, phenylpyruvate) * Autosomal recessive * screened for 2-3 days after birth ( maternal enzyme during birth) * Disorder of aromatic amino acid metabolism--\> musty body odor * Findings: intellectual disability, growth retardation, seizures, fair skin, eczema, musty body ordor * Must avoid aspartame (contains phenylalanine) * Tx: decrease phenylalanine and increase tyrosine in diet

Answer 50

lack of proper dietary therapy during pregnancy * Infant findings * microcephaly * intellectural disability * growth retardation * congenital heart defects

Answer 51

Congenital deficiency of homogentisate oxidase in the degradative pathway of tyrosine into fumarate * Autosomal recessive * Benign disease * Findings * dark connective tissue, brown pigmented sclera, urine turns black on prolonged exposure to air * may have debilitating arthralgias (homogentisic acid toxic to cartilage)

Answer 52

Excess homocysteine * Findings * increase in homocysteine in urine, intellectual disability, osteoporosis, tall stature, kyphosis, lens subluxation, thrombosis, atherosclerosis (stroke, MI) * Homocysteine--\> Methionine * Homocysteine methyltransferase & B12 * Homocysteine --\> Cystathionine--\> Cysteine * Cystathionine synthase & B6 Types * Cysthathionine Synthase deficiency * tx: decrease methionine, increase cysteine, increase B12 and folate in diet * Decreased affinity of cysthathionine synthase for pyridoxal phosphate * Increase B6 and cysteine in diet * Homocysteine methyltransferase deficiency * tx: increase methionine in diet

Answer 53

Hereditary defect of renal PCT and intestinal amino acid transported for Cysteine, Ornithine, Lysine and Arginine (COLA) * Excess cystine in urine can lead to precpitatinof hexagonal cystine stones * Autosomal recessive * Urinary cyanide-nitroprusside test is diagnostic * Tx: * Urinary alkalizination (potassium citrate, acetazolamide) * Chelating agents increase solubility of cystine stones * Good hydration *

Answer 54

Blocked degradation of brached amino acids (Isoleucine Leucine, Valine) * Dereased alpha-ketoacid dehydrogenase * increases alpha-ketoacid in blood * Autosomal recessive * Urine smells like burnt sugar/ maple syrup * Tx: restriction of leucine, isoleucine, valine in diet

Answer 55

Glycogen --\> glucose * Glycogen phosphorylase Glucose --\> Glycogen * Glycogen synthase Regulators * Glucagon: binds glucagon R (liver) * increase cAMP --\> PKA * Activates Glycogen Phosphorylase Kinase * Activates Glycogen phosphorylase * Epi: Binds Beta receptors (liver, muscle) * increase cAMP--\> PKA * activates glycogen phosphorylase kinase * activates glycogen phosphorylase * Epi: binds alpha- receptors (liver) * increase Ca release from ER * activates glycogen phosphorylase kianse * activates glycogen phosphorylase * Insulin: Binds tyrosine kinase dimer R (liver, muscle) * activates Glycogen Synthase * inhibited by PKA * Activates protein phosphatase ( inhibits glycogen Phosphorylase)

Answer 56

* Structure: * branches have a (1,6) bonds * Linkages have a (1,4) bonds * Skeletal muscle * Glycogen undergoes glycogenolysis * glucose 1 P--\> glucose 6P ( exercise) * Hepatocytes * Glycogen is stored and undergoes glycogenolysis to maintain blood sugars * Glycogen phosphorylase cleaves Glu1P residues off until 4 remain (limit dextrin) * 4-alpha-glucanotransferase (debranching enzyme) mvoes three Glu1P from one branch to the linkage * A-1,6 glucosidase cleaves off last Glu1P on branch

Answer 57

* von Gierke disease ( Type I) * Pompe disease ( Type II) * Cori Disease (Type III) * McArdle disease ( Type IV)

Answer 58

* Accumulation of glycogen in cells * Severe fasting glucose, increase glycogen in liver, increase blood lactate, hepatomegaly * Deficiency in Glucose 6 phosphatase * Autosomal recessive * Tx: Frequent oral glucose/ cornstarch, avoid fructose and galactose

Answer 59

* Accumulation of glycogen * Cardiomyopathy * leads to early death * Deficiency: lysosomal a 1,4, glucosidase ( acid maltase-- degradation of glycogen in lysosome) * Autosomal recessive

Answer 60

* Glycogen storage disease * Milder form of von Gierke sxs ( fasting hypoglycemia, increase glycogen in liver, normal blood lactate levels) * Deficiency: Debranching enzyme ( a 1,6 glucosidase) * Autosomal recessive * Gluconeogenesis is intact

Answer 61

* Glycogen storage disease * increase glycogen in muscle but can't break it down * muscle cramps. myoglobinuria (red urine) with strenuous exercise, arrhythmia from electrolyte abnormalities * Deficiency: skeletal muscle glycogen phosphorylase * Autosomal recessive

Answer 62

Caused by deficiency of lysosomal enzymes and leads to accumulation of abnormal metabolites Sphingolipidoses * Fabry disease * Gaucher disease * Niemann-Pick disease * Tay-Sachs disease * Krabbe disease * Metachromatic leukodystrophy Mucopolysaccharidoses * Hurler syndrome * Hunter syndrome

Answer 63

* Lysosomal storage disease * Peripheral neuropathy of hands/ feet, angiokeratoma, cardiovascular/ renal disease * Deficiency: Alpha-galactosidase A * Accumulated substrate: Cermide trihexoside * X-linked Recessive

Answer 64

* Lysosomal Storage disease * Hepatosplenomegaly, pancytopenia, aseptic necrosis of femur, bone crieses * Gaucher cells ( lipid laden macrophage that resembles crumpled tissue paper) * Deficiency: Glucocerebrosidase ( B-glucosidase) * Accumulated substrate: Glucocerebroside * Tx: recombinant glucocerebrosidase * Autosomal recessive

Answer 65

* Lysosomal Storage disease * Progressive neurodegeneration, hepatosplenomegaly, "cherry-red spot" on macula * foam cells (lipid laden macrophages) * Deficiency: Sphingomyelinase * Accumulated substrate: Sphongomyelin * Autosomal recessive

Answer 66

* Lysosomal storage disease * progressive degeneration, developmental delay, cherry-red spot on macula, lysosomes with onion skin * no hepatosplenomegaly ( vs. Niemann-pick) * Deficiency: Hexoaminidase A * Accumulated substrate: GM2 ganglioside * Autosomal recessive

Answer 67

* Lysosomal Storage disease * Peripheral neuropathy, developmental delay, optic atrophy, globoid cells * Deficiency: Galactocerebrosidase * Accumulated substrate: glalactocerebroside, psychosine * Autosomal recessive

Answer 68

* Lysosomal storage disease * Cenral and peripheral demyelination with ataxia, dementia * Deficiency: Arylsulfatase A * Accumulated substrate: Serebroside sulfate * Autosomal Recessive

Answer 69

* Lysosomal storage disease * Developmental delay, gargoylism, airway obstruction, corneal clouding, hepatosplenomegaly * Deficiency: a-L-iduronidase * Accumulated substrate: Heparan sulfate, dermatan sulfate * Autosomal recessive

Answer 70

* Lysosomal Storage disease * Mild Hurler sxs: devo delay, gargoylism, airway obstruction, heptosplenomegaly, with aggressive behavior * Deficiency: Iduronate sulfatase * Accumulated substrate: Heparan Sulfate, dermatan sulfate * X-linked recessive

Answer 71

* Long chain fatty acid degradation requires carnitine-dependant transport into mitchondrial matrix * Deficiency: inability to transport LCFA into mitochondria resulting in toxic accumulation * Causes weakness, hypotonia, hypoketotic hypoglycemia

Answer 72

* Increase dicarboxylic acids * decrease glucose and ketones * decreased acyl-coA--\> decrease fasting glucose

Answer 73

* Citrate (citrate shuttle: mito --\> cyto) * Acetyl-coA ( ATP citrate lyase) * Malonyl Co-A * Fatty acid synthesis ( Palmitate)

Answer 74

* Fatty acid + CoA * Acetyl CoA ( Fatty acid CoA Synthetase) * Carnitine Shuttle ( Cyto to mitochondria) * Beta- oxidation of acyl CoA to acetyl CoA groups * Ketone bodies * TCA cycle

Answer 75

* Liver * Fatty acids and amino acids are metabolized to acetoacetate and B-hydroxybutyrate * breath smells like acetone ( fruity) * Urine test does not detect B-hydroxybutyrate * Prolonged starvation, diabetic ketoacidosis * oxaloacetate is depleted for gluconeogenesis * Alcoholism * excess NADH shunts oxaloacetate to malate * Leads to build of acetyl-CoA * shunts glucose and FFA to production of ketone bodies

Answer 76

* Fed state * Glycolysis and aerobic respiration * _Insulin_ stimulates storage of lipids, proteins, fats * Fasting (in between meals) * Hepatic glycogenolysis * Hepatic gluconeogenesis * Adipose release of FFA * _Glucagon, adrenaline_ stimulates use of fuel reserves * Starvation (1-3 days) * Hepatic glycogenolysis * Adipose release FFA * Muscle and liver shift fuel use from glucose to FFA * Hepatic gluconeogenesis from tissue lactate and alanine & from adipose tissue glyerol and propionyl coA (odd chain FA) * Glycogen reserves depleted after 1 day * Starvation after day 3 * Adipose stores (ketone bodies) become main source of energy for brain * after depletion, vital protein degradation occurs leading to organ failure and death

Answer 77

* Rate limiting step: HMG-CoA reductase * induced by insulin * HMG-CoA --\> mevalonate * 2/3 of plasma cholesterol is esterified by lecithin-cholesterol acyltransferase (LCAT) * Statin competitively and reversibly inhibit HMG-CoA reductase

Answer 78

* Dietary fat & cholesterol absorbed from intestine * Chylomicrons transport lipids * LDL: lipoprotein lipase degrades TG circulating in chylomicrons to FFA and remnants * FFA * is stored in adipose * take up by peripheral tissues with LDL Receptors * Chylomicron remnants * take up by liver * Liver synthesizes VLDL ( delivery to tissues) * LPL degrades TG in VLDL to form FFA and IDL * IDL is degraded by Hepatic Lipase (TG) to LDL * IDL is take up by hepatic LDL R

Answer 79

* Liver/ intestine make nascent HDL * LCAT catalyzes the esterification of cholesterol to mature HDL * Cholesterol ester transfer protein (CETP) transfers cholesterol esters to VLDL, IDL, LDL

Answer 80

* E: mediates remnant uptake * chylomicrons, chylomicron remnant, VLDL, IDL, HDL * AI: activates LCAT * chylomicron, VLDL, HDL * CII: Lipoprotein lipase cofactor * Chylomicrons, VLDL, HDL * B48: mediates chylomicron secretion * Chylomicron, chylomicron remnant * B100: binds LDL receptor * VLDL, IDL, LDL

Answer 81

* Composed of cholesterol, TG, phospholipids * LDL: transport cholesterol from liver to tissues * HDL: transport cholesterol from periphery to liver

Answer 82

* apolipoproteins: E, AI, CII, B48 * delievers TG to peripheral tissues * delievers choelsterol to liver in form of chylomicron remnants * secreted by intestinal epithelial cells

Answer 83

* Apolipoproteins: E, CII, B100 * Delievers hepatic TG to peripheral tissues * Secreted by the liver

Answer 84

* Apolipoproteins: E, B100 * Formed in the degradation of VLDL * Delivers TG and cholesterol to liver

Answer 85

* apolipoproteins: B100 * delivers hepatic cholesterol to peripheral tissues * formed by hepatic lipase modification of IDL in peripheral tissue * taken up by cells via receptor mediated endocytosis

Answer 86

* Apoplipoproteins: E, A1, CII * mediates reverse cholesterol transport from periphery to liver * acts as repository for apoC and ApoE ( for chylomicron and VLDL metabolism) * Secreted from liver and intestine * alcohol increase synthesis

Answer 87

* Deficiency: Lipoprotein Lipase or altered CII * Autosomal recessive * increased: chylomicrons, TG, cholesterol * causes pancreatitis, hepatosplenomegaly, eruptive/ pruritic xanthoma

Answer 88

* absent or defective LDL receptor * Increased: Cholesterol, LDL * Autosomal Dominant * Accelerated atherosclerosis * may have MI before age 20 * tendon (achilles) xanthoma * corneal arcus

Answer 89

* Hepatic overproduction of VLDL * Increased: VLDL, TG * Autosomal Dominant * Causes pancreatitis

Answer 90

* Gram positive * Catalase positive * Cluster * Cocci

Answer 91

* Novobiocin sensitive * Coagulase negative * Catalase Positive * Cocci * Gram +

Answer 92

* Novobiocin resistant * coagulase negative * catalase positive * Cocci * Gram positive

Answer 93

* Capsule * optochin sensitive * bile soluble * alpha hemolysis * Catalase negative * cocci, chains * Gram positive

Answer 94

* no capsule * optochin resistant * bile insoluble * alpha hemolytic * cocci, chains * Gram +

Answer 95

* Bacitracin sensitive * Beta hemolytic * cocci, chains * catalase negative * Group A strep * Gram positive

Answer 96

* Group B strep * Bacitracin resistant * Beta hemolysis * catase negative * cocci, chains * gram positive

Answer 97

* Group D * Growth in bile and 6.5% NaCl ( E. faecalis) * gamma hemolytic ( no hemolysis) * catase negative * cocci, chains * Gram positive

Answer 98

* non-enterococcus * grows in bile * does not grow in 6.5% NaCl * Gamma hemolytic ( no growth) * Catalase negative * chains, cocci * gram positive

Answer 99

* Anaerobe * not acid fast * branching filaments gram positive

Answer 100

* aerobe * acid fast * branching filaments * gram positive

Answer 101

* Strep pneumoniae * Viridans streptococci ( S. mutans)

Answer 102

Forms clear areas of hemolysis on blood agar * Staphylococcus aureus * Streptococcus pyogenes * Streptococcus agalactiae * Listeria monocytogenes

Answer 103

* Maltose fermenter * Diplococci * Gram negative

Answer 104

* maltose non-fermenter * diplococci * gram negative

Answer 105

* H. influenzae * pasteurella * Brucella * Brodetella pertussis

Answer 106

* Klebsiella * E. Coli * Enterobacter

Answer 107

* Citrobacter * Serratia

Answer 108

* Shigella * salmonella * proteus * yersinia

Answer 109

Pseudomonas

Answer 110

* Grows in 42C * oxidase positive * comma shaped * gram negative

Answer 111

* Grows in alkaline media * oxidase positive * common shaped * gram negative

Answer 112

* produces urease * oxidase positive * comma shaped * gram negative