random Flashcards

1
Q

other sugars

A

erythritol - artificial sweetner, 4 C, not much flatulence
xylitol - 5 C, natural sweetner, flatulence with lots of consumption
mannitol - used for hand injury, kidney issues, helps drugs pass BBB, helps with CF
sorbitol - found in gum, toothpaste, mouthwash, laxative, can cause catarcts or neuropathy in diabetics

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2
Q

glutathione

A

antioxidant, found in cytosol

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3
Q

3 membrane lipids

A

cholesterol, glycolipids, phospholipids

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4
Q

3 glycerophospholipids

A

phosphatidylcholine, phosphatidylserine, phosphatidylinositol

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5
Q

lipid rafts

A

made of cholesterol, important for cell signaling

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6
Q

what do ligand gated ion channels have to do with alzheimer’s disease?

A

glutamate is excessively released in dying brain cells. glutamate receptor antagonist helps pts (Mimantine/Namenda)

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7
Q

in P-type ATPases (one type of primary active transport) what aa residue gets phosphorylated?

A

aspartate

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8
Q

Pb (lead) poisoning caused by what? treatment?

A

Pb inhibits ferrochelatase (coenzyme of hemoglobin), so heme can’t be made. Give pt Ca-EDTA bc Pb has higher affinity for EDTA. Pb-EDTA will be excreted in urine.

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9
Q

allosteric effector, proenzymes, and isozymes?

A

allosteric effectors can change shape of enzyme to fit substrate (+) or make enzyme’s shape not fit substrate (-_.

proenzymes are zymogens, typically proteolytic. need peptide bond cleavage to become activated.

isozymes act on the same substrate as original enzymes but they have different kinetic properties (Km, Vmax, etc) and diff binding sites/aa sequences.

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10
Q

what isozymes act as markers for MI by being elevated in the blood?

A

isozymes of lactate dehydrogenase, creatine kinase, and AST

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11
Q

troponin subunits? what troponin subunit is elevated after MI?

A

Tn-T (tropomyosin), Tn-C (calcium), Tn-I (inhibitory). After MI, cTn-I increased (cardiac troponin). Troponin has overtaken isozymes to detect MI.

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12
Q

Fanconi-Bickel syndrome

A

GLUT2 transporter mutation so can’t uptake glucose, galactose, and fructose

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13
Q

clinical markers of hemolytic anemia

A

increased lactate dehydrogenase, bilirubin

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14
Q

high fructose corn syrup + obesity link

A

since fructose bypasses PFK1, is unregulated, and joins in glycolysis as an intermediate, you end up with a lot of pyruvate that turns into a lot of acetyl coA. With too much acetyl coA, too much fat synthesis.

can lead to insulin resistance (diabetes 2) and fatty liver

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15
Q

oxidative phase of PPP (non reversible phase)

A

making glucose 6 P into ribulose 5 P with glucose 6 P dehydrogenase. this step generated 2 NADPHs. When you have an infection, you need NADPH. so if there’s a problem with glucose 6 dehydrogenase, you can’t make NADPH. NADPH regenerates glutathione, which detoxifies H2O2. cancer prefers this pathway bc need ribose which comes from ribulose.

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16
Q

non-oxidative phase (reversible)

A

end products (ribose, fructose, glyceraldehyde) go to nucelotide pathways, glycolytic pathways, and gluconeogetic pathways. Infections prefer this pathway bc they want NADPH. if you make frucose and glyceraldehyde, they can undergo nucleogenesis and make glucose 6 P for oxidative phase (which produces 2 NADPHs).

17
Q

hyperthyroidism is due to what

A

thyroidglobulin (thyroid makes this, it’s made from many Tyr resides, some which are ii and some i) makes T3 (Tyri + Tyrii) and T4 (Tyrii + Tyrii). Too much T3 and T4 leads to hyperthyroidism. Txt: take agents that block iodination of thyroidglobulin, hence decreasing amount ot T3 and T4.

18
Q

what two enzymes need PLP in what two rxns

A
  1. CBS needs it to break down homocysteine

2. alanine amino transferase needs it to make pyruvate into alanine

19
Q

heart wants energy from what biomcules?

skeletal muscle wants energy from what biomcules?

A

heart - glucose, lactate, FA

skeletal muscle - glucose, FA, aas

20
Q

for metabolic syndrome you need one of? two of?

A

one of: insulin resistance, impaired glucose tolerance, impaired fasting glucose, diabetes

two of: BP over 140/90 or on BP meds, microalbuminuria, dyslipidemia (more LDL, less HDL), central obesity

21
Q

inborn errors of metabolism

A

x linked, mitochondrial inheritance, autosomal dominant/recessive

22
Q

orotic aciduria occurs if what?

A

UMP synthase doesn’t work

23
Q

in BCAA catabolism, what becomes what?

A

Val (glucogenic) and Ile (both) becomes succinyl coA. Leu (ketogenic) becomes acetyl coA.

24
Q

in the brain, what fixes ammonia?

A

glutamate dehydrogenase

25
Q

what does coenzyme A do?

A

activates acyl groups (like acetyl coA), forms high energy thioester linkages

26
Q

what does arsenite do?

A

modifies lipoic acid, so affects PDC. also affects a-ketoglutarate dehydrogenase, and a-keto acid dehydrogenase.

27
Q

if PDC doesn’t work, what happens?

A

you get pyruvate build up, and then lactic acidosis. avoid alanine, bc alanine can turn into pyruvate.

28
Q

how does rat poison work (fluoroacetate)?

A

fluoroacetate + acetyl coA becomes fluoroacetyl coA which becomes fluorocitrate (analog of citrate, inhibits aconitase). citrate builds up, negatively inhibiting citrate synthase. STOPS TCA CYCLE

29
Q

succinyl coA + glycine = ?

A

ALA (first step in heme synthesis)

30
Q

anapleurotic rxns in TCA cycle

anabolic rxns in TCA cycle

A

anapleurotic

fasting: proteins degrade to aas, which make OAA, fumarate, succinyl coA, and a-ketoglutarate
fed: carboxylation of pyruvate (make OAA) to make TCA cycle run

anabolic

  1. OAA makes glucose via gluconeogenesis
  2. citrate activates acetyl coA carboxylase (fatty acid synthesis)
  3. OAA + a-ketoglutarate make aas.
31
Q

2-oxoglutaric acid aciduria

A

neural deficit, diagnosed with urine test

32
Q

fumarase deficiency

A

neural deficity, diagnosed with urine test, encephalopathy, speech delay, fatal

33
Q

succinyl coA synthetase (SCS) deficiency

A

mutations in 2/3 subunits that make up enzyme, direct genetic testing

34
Q

ferredoxin

A

small proteins that serve as electron carriers in mitochondrial/cytochrome systems

ferredoxin 1: biosynthesis of steroid hormones, metabolism of vitamin D and bile acids
ferredoxin 2: biosynthesis of heme, proteins