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Biochem Flashcards

1
Q

Desmin stain

A

Muscle

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2
Q

Cytoskeleton stain

A

Epithelial cells

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3
Q

Gfap

A

Neuro glia

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4
Q

Neurofilaments

A

Neurons

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5
Q

I cell disease

A

Deficient mannose-6-phosphate

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6
Q

Which way do Dynein and kinesin move?

A

Dynein moves retrograde (+ to -) and kinesin moves anterograde (- to +)

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7
Q

What does ouabain do?

A

Inhibits the na/k pump by binding to the K+ site

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8
Q

Where does hydroxyl action of collagen occur?

A

In the RER, specific proline and lysine residues are hydroxylated. Requires vitamin c (deficiency causes scurvy)

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9
Q

Where does glycosylation and the forming of collagen triple helices occur

A

In the RER. Problems firming this helix lead to osteogenesis imperfect a

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10
Q

What is Menkes disease?

A

X linked recessive connective tissue disease caused by impaired copper absorption and transport due to defective Menkes protein. Leads to decrease activity of Lysol oxidase

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11
Q

What is RNA interference?

A

DsRNA is synthesized that is complementary to the mRNA sequence of interest. When transfected into human cells, dsRNA separates and promotes degradation of target mRNA, “knocking down” gene expression

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12
Q

What is special about the inheritance of alpha-1 anti trypsin deficiency

A

The alleles are co-dominant

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13
Q

What is heteroplasmy?

A

Presence of both normal and mutated mtDNA, resulting in variable expression in mitochondria lily inherited disease

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14
Q

Vimentin stain

A

Connective tissue

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15
Q

Enzymes that use thiamine

A

Pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, transketolase, branched-chain ketoacid dehydrogenase

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16
Q

Reactions vitamin B2 is used in

A

(Riboflavin) Used as cofactors in redox reactions, eg, the succinate dehydrogenase reaction in the TCA cycle

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17
Q

How is niacin made?

A

Derived from tryptophan. Requires B2 and B6.

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18
Q

How can you get a deficiency of niacin?

A

Hartnup disease (decreased tryptophan absorption), malignant carcinoid syndrome (increased tryptophan metabolism), and isoniazid (decreased vitamin B6)

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19
Q

What reactions is B5 needed for?

A

(Pantothenic acid) Essential component of coenzyme A (CoA, a cofactor for acyl transfers) and fatty acid synthase

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20
Q

What is B6 used for?

A

Converted to pyridoxal phosphate (PLP), a cofactor used in transamination (eg. ALT and AST), decarboxylation reactions, glycogen phosphorylase. Synthesis of cystathionine, heme, niacin, histamin, and neurotransmitters including serotonin, epi, norepi, dopamine, and GABA

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21
Q

What is B7 used for?

A

(Biotin) Cofactor for carboxylation enzymes: pyruvate carboxylase, acetyl-CoA carboxylase, propionyl-CoA carboxylase

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22
Q

How can you get a deficiency of biotin?

A

Antibiotic use or excessive digestion of raw egg whites.

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23
Q

What reaction is B12 needed for?

A

Homocysteine to Methionine (homocysteine methyltransferase) and Methylmalonyl-CoA to Succinyl-CoA (methylmalonyl-CoA mutase [isomerase])

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24
Q

Interaction between Vitamin C and iron

A

Vitamin C facilitates iron absorption by reducing it to Fe2+ state

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25
Q

What is Vitamin C necessary for?

A

Hydroxylation of proline and lysine in collagen synthesis; necessary for dopamine beta-hydroxylate, which converts dopamine to NE

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26
Q

Rosary chest

A

Rickets (vitamin D deficiency in children)

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27
Q

Type of anemia in vitamin E deficiency

A

Hemolytic

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28
Q

Lab values in vitamin K deficiency

A

Increased PT and aPTT but normal bleeding time

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29
Q

Zinc deficiency

A

Delayed wound healing, hypogonadism, decreased adult hair, dygeusia, anosmia, acrodermatits enteropathica. May predispose to alcoholic cirrhosis

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30
Q

Liver findings in kwashiorkor

A

Fatty change due to decreased apolipoprotein synthesis

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31
Q

Ethanol metabolism

A

Ethanol to acetaldehyde by alcohol dehydrogenase (in the cytosol); then acetaldehyde to acetate be acetaldehyde dehydrogenase (in the mitochondria)

32
Q

What is fomepizole

A

Inhibits alcohol dehydrogenase and is an antidote for methanol or ethylene glycol poisoning

33
Q

What is disulfiram

A

Inhibits acetaldehyde dehydrogenase

34
Q

What is the limiting reagent in ethanol metabolism

A

NAD+

35
Q

What changes does ethanol metabolism cause?

A

Increases the NADH/NAD ratio in the liver, causing: pyruvate to go to lactate, oxaloacetate to go to malate (preventing gluconeogenesis-> fasting hypoglycemia), and dihydroxyacetone phosphate to of to glycerol-3-phosphate (combines with fatty acids to make triglycerides causing hepatosteatosis). NADH/NAD ratio also disfavors TCA production of NADH causing increased utilization of acetyl-CoA for ketogenesis and lipogenesis

36
Q

Ethanol can be metabolized in the peroxisome by what enzyme?

A

Catalase

37
Q

Ethanol can be metabolized in the microsome by what enzyme?

A

CYP2E1 (creates ROS)

38
Q

What regulates glycogen synthase?

A

Positive regulation: glucose-6-phosphate, insulin, and cortisol; negative regulation: epinephrine and glucagon

39
Q

What regulates the HMP shunt

A

Positive: NADP+, Negative: NADPH

40
Q

What regulates glycolysis?

A

Positive: AMP, fructose-2-bisphosphate, Negative: ATP, citrate

41
Q

What regulates gluconeogenesis?

A

Positive: ATP, acetyl-CoA; Negative: AMP, fructose-2,6-bisphosphate

42
Q

What regulates fatty acid synthesis?

A

Positive: insulin, citrate; negative: glucagon, palmitoyl-CoA

43
Q

What regulates fatty acid oxidation?

A

Negative: Malonyl-CoA

44
Q

Effect of arsenic on glycolysis

A

Causes it to produce zero net ATP

45
Q

When are NAD+ and NADPH used?

A

NAD+ is used in catabolic process to carry reducing equivalents away as NADH; NADPH is used in anabolic processes as a supply of reducing equivalents

46
Q

Hexokinase vs glucokinase

A

Hexokinase- most tissues, low Km (higher affinity), low Vmax (lower capacity), not induced by insulin; glucokinase- liver and beta cells of pancreas, higher Km (lower affinity), high Vmax (higher capacity), induced by insulin

47
Q

Vomiting, rice-water stools, garlic breath

A

Arsenic poisoning (arsenic inhibits lipoic acid)

48
Q

How many ATP are produced per NADH/ FADH2

A

1NADH=2.5 ATP, 1 FADH2 = 1.5 ATP

49
Q

What does Rotenone block

A

Complex 1 of the electron transport chain

50
Q

What does antimycin A block

A

Complex III of the electron transport chain

51
Q

What does oligomycin block?

A

Complex V of the electron transport chain. An ATP synthase inhibitor. Directly inhibits mitochondrial ATP synthase, causing an increased proton gradient. No ATP is produced because electron transport stops

52
Q

What blocks complex IV?

A

Cyanide, CO

53
Q

Irreversible enzymes of gluconeogenesis

A

Pyruvate carboxylase, phosphoenolpyruvate carboxykinase, fructose-1,6-bisphosphatase, glucose-6-phosphatase

54
Q

What does pyruvate carboxylase require? What activates it?

A

Biotin, ATP. Activated by acetyl-CoA

55
Q

What does PEP CK require?

A

GTP

56
Q

What regulates fructose-1,6-bisphosphatase?

A

Pos: citrate; neg: fructose-2,6-bisphosphate

57
Q

What is NADPH required for?

A

Glutathione reduction inside RBCs, fatty acid and cholesterol biosynthesis

58
Q

Where does the HMP shunt take place?

A

Lactating mammary glands, liver, adrenal cortex (sites of fatty acid or steroid synthesis), RBCs

59
Q

What is a copper reaction test?

A

Nonspecifically detects the presence of reducing sugar

60
Q

Genetics of essential fructosuria

A

Autosomal recessive, involves a defect in fructokinase

61
Q

Fructose intolerance

A

Autosomal recessive, deficiency of aldolase B. Fructose-1-P accumulates causing a decrease in available phosphate which results in inhibition of glycogenolysis and gluconeogenesis.

62
Q

Treatment of fructose intolerance

A

Decrease intake of both fructose and SUCROSE (glucose + fructose)

63
Q

What may present as a failure to track objects or to develop a social smile?

A

Galactokinase deficiency, galactitol accumlates, causing cataracts. Autosomal recessive

64
Q

FTT, jaundice, hepatomegaly, infantile cataracts, intellectual disability. Can lead to E. coli sepsis in neonates

A

Classic galactosemia, absence of galactose-1-phosphate uridyltransferase, AR

65
Q

Tx of galactosemia

A

Exclude galactose and lactose (galactose and glucose) from the diet

66
Q

Which cells have only aldose reductase?

A

Schwann cells, retina, and kidneys

67
Q

What is an alternative method of trapping glucose in the cell?

A

Converting it to its alcohol counterpart, sorbitol, via aldose reductase (requires NADPH)

68
Q

What happens to sorbitol?

A

Some tissues (liver, ovaries, and seminal vesicles) have sorbitol dehydrogenase (requires NAD+) that can convert it to fructose

69
Q

Diagnosing lactase deficiency

A

Stool demonstrates decreased pH and breath shows increased hydrogen content with lactose tolerance test. Intestinal biopsy shows NORMAL mucosa

70
Q

Which amino acids are acidic?

A

Aspartic acid and glutamic acid

71
Q

Which amino acids are basic?

A

Arginine, lysine, histidine

72
Q

Treatment of pyruvate dehydrogenase complex deficiency?

A

Increase intake of ketogenic nutrients (e.g., high fate content or increased lysine and leucine)

73
Q

What are the essential amino acids?

A

Methionine, valine, histidine (glucogenic). Isoleucine, phenylalanine, threonine, tryptophan (glutogenic/ketogenic). Leucine, lysine (ketogenic)

74
Q

Urea cycle

A

CO2+NH3 goes to carbamoyl phosphate in the rate limiting step. (Required cofactor: N-acetylglutamate) Then carbamoyl phosphate combines with ornithine to make citrulline. Citrulline + aspartate = argininosuccinate. Fumarate leaves-> arginine. Organize converts this to urea and ornithine

75
Q

What is the Cori cycle?

A

Glucose to pyruvate to lactate (moves to liver) to pyruvate to glucose (moves to tissue)

76
Q

What is the Cahill cycle?

A

Glucose in the muscle to pyruvate to alanine (moves to liver) to pyruvate back to glucose (moves to muscle)

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