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Biochemistry (W) > Biochem UWorld 1 > Flashcards

Biochem UWorld 1 Flashcards

0
Q

Rate of metabolism of glycolysis for glucose, galactose, mannose, sucrose, fructose

A

Glucose, galactose, and mannose enter glycolysis before PFK-1 step, so their rates of metabolism are limited. Sucrose –> fructose enter downstream, and so are not affected by PFK-1

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1
Q

Rate limiting step in glycolysis

A

Phosphofructokinase-1 (F-1-P –> F-1,6-BP)

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2
Q

Septic shock and lactic acidosis

A

Causes lactic acidosis. Tissue hypoxia –> impaired oxidative phosphorylation, shunting of pyruvate to lactate

Decrease in clearance of lactic acid in hepatic hypoperfusion also contributes

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3
Q

What is the likely mechanism for a protein with closely packed alpha helices containing isoleucine, valine, alanine, methionine, phenylalanine?

A

These are all non-polar hydrophobic aa’s –> spans plasma membrane

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4
Q

AA’s with 3 titratable protons

A

Histidine, arginine, lysine aspartic acid, glutamic acid, cysteine, tyrosine.

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5
Q

Cellular metabolism that occurs in the mitochondria

A

b-oxidation of fatty acids, ketogenesis, TCA cycle, part of urea cycle, pyruvate decarboxylation

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6
Q

Where to the reactions of the pentose phosphate pathway take place?

A

cytoplasm

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7
Q

What are the two purposes of the HMP shunt (pentose phosphate pathway)?

A

1) Generation of NADPH for reductions

2) Generates ribose for nucleotide synthesis

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8
Q

What are the two stages of the pentose phosphate pathway?

A

1) oxidative/irreversible: G-6-P –> Ribulose-5-P + CO2 + 2NADPH via G-6-p dehydrogenase
2) Nonoxidative (reversible): ribulose-5-p Ribose-5-p + G3P + F6P, via phosphopentose isomerase, transketolases

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9
Q

What enzymes is lipoic acid a cofactor for? What does deficiency cause?

A

Pyruvate dehydrogenase (gets pyruvate from glycolysis to acetyl-coa and TCA cycle), a-ketoglutarate dehydrogenase (TCA cycle), branched chain ketoacid dehydrogenase (degrades isoleucine, leucine, valine)

Pyruvate DH deficiency = lactic acidosis, branched chain ketoacid DH deficiency causes maple syrup urine disease

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10
Q

Infant develops vomiting and lethargy several days after birth. Hypertonicity, muscle rigidity. Odor of burnt sugar in diaper. Dx, and what AAs should you restrict?

A

Maple syrup urine disease, restrict isoleucine, leucine, valine

I Love Vermont Maple Syrup

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11
Q

What does irradiation do to cancer?

A

1) DNA double stranded breakage

2) Free radical formation

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12
Q

What vitamin helps in treatment measles?

A

Vitamin A

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13
Q

Vitamin A deficiency

A

Night blindness (nyctalopia), dry scaly skin (xerosis cutis), alopecia, corneal degeneration (keratomalacia), immune suppression

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14
Q

8 y/o losing previously acquired motor skills, hepatosplenomegaly, leukocytes with prominent intracellular sphingomyelin accumulations

A

Niemann-Pick disease

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15
Q

Niemann-pick disease: inheritance, deficient enzyme, accumulated substrate.

A

Autosomal recessive, deficiency in sphingomyelinase leads to accumulation of sphingomyelin

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16
Q

Tay-Sachs disease findings

A

Progressive neurodegeneration and developmental delay, cherry red spot on macula, NO hepatosplenomegaly, lysosomes with onion skin

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17
Q

Tay-sachs: inheritance, deficient enzyme, accumulated substrate

A

Autosomal recessive deficiency in hexosaminidase A leads to accumulation of GM2 ganglioside

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18
Q

What are spliceosomes made of and what do they do?

A

Made of snRNPs plus proteinsproteins. Involved in splicing out introns.

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19
Q

Ehlers-Danlos syndrome

A

Type III and V collagen (actually many types)

Over-flexible joints, over-elastic skin, fragile tissue susceptible to bleeding and bruising, berry and aortic aneurysm

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20
Q

How does TNF-alpha induce insulin resistance? What else can do this?

A

Activates serine kinases, and serine phosphorylation blocks tyrosine phosphorylation and blocks downstream signaling.

Aberrant phosphorylations also occur with catecholamines, glucocorticoids, and glucagon.

21
Q

What kind of cell signaling does insulin go through?

A

PI3K to glycogen, lipid, and protein synthesis

RAS/MAP kinase pathway to cell grown and DNA synthesis

22
Q

Reducing sugars

A

fructose, galactose, glucose

23
Q

Essential fructosuria

A

Benign deficiency in fructokinase (fructose to F1P)

24
Q

Hereditary fructose intolerance

A

AR deficiency of Aldolase B –> buildup of F1P and decrease in available phosphate, inhibits glycogenolysis and gluconeogenesis.

Hypoglycemia, jaundice, cirrhosis, vomiting following consumption of juice, honey, and fruit.

25
Q

What is a source of NADPH? What does it do?

A

Get it from the HMP shunt. Necessary for anabolic reactions that use NADPH as electron donor, such as fatty acid, cholesterol, and sterol synthesis as well as drug metabolism. Also used to reduce glutathione –> repair oxidative damage to RBCs.

26
Q

G6P Dehydrogenase deficiency

A

X-linked recessive, associated with malaria resistance. Low NADPH leads to poor RBC defense against oxidizing agents (fava beans, sulfonamides, primaquine, anti-TBs, free radicals from infection).

27
Q

G6PD Deficiency - blood smear findings

A

Hemolytic anemia with heinz bodies (oxidized Hb precipitates) and bite cells (from phagocytosis of Heinz bodies by splenic macrophages)

28
Q

Vitamin A overdose

A

Acute: nausea, vomiting, vertigo, blurred vision
Chronic: alopecia, dry skin, hyperlipidemia, hepatotoxicity, hepatosplenomegaly, vision problems, intracranial hypertension
Teratogenic: cleft palate, micrcephaly, cardiac defects

29
Q

Hepatic encephalopathy biochemistry

A

Increased ammonia and neurotoxins when liver can’t metabolize waste products. Affects glutamate-glutamine cycle, increasing levels of glutamine. Causes buildup of glutamine in astrocytes, decreased brain glutamate stores. Metabolized by alphaketoglutarate = less for Krebs cycle = reduced energy.

30
Q

Vitamin C (ascorbic acid) deficiency

A

Scurvy: collagen synthesis defect. Swollen gums, bruising, hemarthrosis, anemia, poor wound healing, hemorrhages, hematomas, weakened immune responses

31
Q

Young child with intellectual disability, seizures, hypopigmentation. Deficiency of what enzyme? What has built up?

A

Phenylalanine hydroxylase –> phenylalanine excess and tyrosine deficiency. Phenylketonuria

32
Q

Why does PKU cause hypopigmentation? Musty odor? Inheritance pattern? When does it present?

A

Autosomal recesive. High phenylalanine inhibits melanin synthesis from DOPA (which comes from tyrosine). Presents gradually after birth, after mom’s enzymes go away

33
Q

Coenzymes required for branched chain a-ketoacid dehydrogenase. Similar enzymes

A

Thiamine pyrophosphate, lipoate, CoA, FAD, NAD (TLC For Nancy)

Similar to pyrovate dehydrogenase and a-ketoglutarate dehydrogenase

34
Q

3 enzymes used to metabolize fructose

A

Fructose to F1P via fructokinase (essential fructosuria, benign)
F1P to DHP and glyceraldehyde via Aldolase B (fructose intolerance)
Glyceraldehyde to G3P via triokinase (to glycolysis)

35
Q

Baby with vomiting, jaundice, cirrhosis, irritability since starting to drink juices. Dx, missing enzyme

A

Fructose intolerance, aldolase B

36
Q

Xeroderma pigmentosa

A

Deficiency of UV-endonucleases which fix thymidine dimers. Autosomal recessive, photosensitivity, poikiloderma, hyperpigmentation in sun-exposed areas.

37
Q

Pt with hypoxia induced metabolic acidosis, increased anion gap, high plasma lactate. Low activity of which enzyme?

A

Low activity of pyruvate dehydrogenase (which normally sends pyruvate to ox-phos pathway) and high activity of lactate dehydrogenase (sends to anaerobic respiration)

38
Q

Cells with lots of smooth ER probably do what? Found where

A

Contain enzymes for steroid and phospholipid synthesis. Synthesis of steroids, cholesterol. Seen in adrenals, gonads, liver eg

39
Q

P bodies

A

Proteins in the cytoplasm that mRNAs can occasionally interact with. Involved in regulation and turnover, can also be involved in storage.

40
Q

Where do post translational modifications (5’ cap, 3’-polyA tail, intron excision) occur?

A

Nucleus

41
Q

What is a transamination? What is an essential cofactor for these reactions?

A

Transfer of amino group from amino acid to a-keto acid, making an amino acid. Requires pyroxidine (B6)

eg oxaloacetate + glutamate –> aspartate + a-ketoglutarate

42
Q

What 2 reactions is pyroxidine pyrophosphate (B6) used in?

A

Transaminations and decarboxylations

43
Q

E. coli lac operon

A

Codes for proteins necessary for lactose metabolism. Polycistronic - one mRNA codes for several proteins. Regulated by single promotor, operator, and set of regulatory elements

44
Q

What protein to fibroblasts make in a triple helix? What is the most common AA?

A

Collagen. Every third AA is glycine. Proline is also necessary, but not as common.

45
Q

Degradation of triglycerides

A

TG –lipase–> glycerol + FFA

Glycerol –glycerol kinase(liver)–> glycerol-3-P –> DHAP –> energy via glycolysis or glucose via gluconeogenesis

FFA –> beta oxidation/ketogenesis

46
Q

What tissue can use triglyceride degradation products to make energy or glucose?

A

Liver can use glycerol kinase to make glycerol into DHAP, a substrate for glycolysis or gluconeogenesis

47
Q

Elastin - what 3 AA’s is it made of primarily? Hydroxylation state?

A

Primarily glycine, alanine, valine. Also has some proline and lysine, but not very hydroxylated

48
Q

How are elastin and collagen different?

A
  1. Proline and lysine are very hydroxylated in collagen, much less in elastin
  2. Collagen makes triple helices with hydroxylation, glycosylation, disulfide bridges
  3. Elastin’s recoil comes from desmosine crosslinking between lysines
49
Q

How is the lac operon regulated?

A
  1. negative: binding of repressor protein to operator locus

2. positive: c-AMP-CAP binding upstream from promotor region

Biochemistry (W) (3 decks)

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