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Renal Exam #1 > Nitrogen Metabolism > Flashcards

Nitrogen Metabolism Flashcards

1
Q

The first step in nitrogen metabolism is:

Via which enzyme:

A

Oxidative deamination via glutamate dehydrogenase

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2
Q

Urea cycle

A

Asp + citrulline –> arginosuccinate –> fumarate (goes to TCA) + Arg –> urea and ornithine (+carbamoyl phosphate) –> citrulline

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3
Q

What is the carbon skeleton source for urea cycle reactions?

A

Aspartate

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4
Q

What cannot be resorbed in Hartnup’s?

In cystinuria?

A

Nonpolar AAs

Dibasic AAs

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5
Q

Why is Hartnup’s and Cystinuria a “double whammy” in a sense?

A

There is poor absorption in both the intestines and malabsorption.

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6
Q

Where does reabsorption of AA and Glc occur?

A

In the PCT

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7
Q

What gene/protein function in reuptake of Glc and AA?

A

SLC

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8
Q

Hartnup’s Disease has poor absorption which AAs?

A

Nonpolar

Ala, Ser, Thr, Val, Leu, Ile, Phe, Tyr, Trp, Gln, Asn and His

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9
Q

How does HD manifest? (5)

A 
Infancy to thrive as an infant
Nystagmus
Ataxia
Photosensitivity
Pellegra
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10
Q

What is the treatment for HD generally? (3)

A

Niacin w/ a high protein diet and nicotinamide supplementation.

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11
Q

Trp pathway

A

Trp –> niacin –> NAD+/NADP+

Trp –> 5-hydroxytrptophan –> serotonin –> melatonin

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12
Q

How does niacin help in HD?

A

The de novo pathway does not work due to malabsorption of Trp.
Therefore, Niacin can convert to NAD+/NADP+

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13
Q

What are “dibasic” AAs? (4)

A 
COAL
Cys
Orn
Arg
Lys
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14
Q

What doe patients present with in cystinuria? (2)

A

Renal crystals

Renal colic

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15
Q

Draw the Phe to Fumarate pathway

A

Phe –> Tyr –> p-Hydroxyphenylpyruvate –> homogentisate –> Maleylacetoacetate –> Fumarylacetoacetate –> Fumarate

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16
Q

Type II tyrosinemia occurs from:

Enzyme

A

From Tyr –> p-Hydroxyphenylpyruvate

tyrosine aminotransferase

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17
Q

Type III tyrosinemia occurs from:

Enzyme

A

p-Hydroxyphenylpyruvate –> Homogentisate

p-hydroxypyruvate oxidase

18
Q

Alkaptonuria occurs from:

Enzyme

A

Homogentisate –> Maleylacetoacetate

homogentisate oxidase

19
Q

Type I tyrosinemia occurs from:

Enzyme

A

Fumarylacetoacetate –> fumarate

fumarylacetoacetate hydrolase

20
Q

PKU is a defect in which enzyme?

A

PAH

Phenylalanine hydroxylase

21
Q

Instead of being metabolized normally to Tyr, what happens to Phe in PKU?

A

Phe –> phenylpyruvate –> phenylacetate

22
Q

PKU disrupts what physiologically?

A

Neurotransmission and blocks AA transport in the brain.

23
Q

Secondary PKU results from:

A

BH4 deficiency (a cofactor of PAH).

24
Q

What test tests for PKU?

A

Guthrie test

25
Q

PKU must be found when?
What levels of blood Phe are concerning?
Treatment of PKU

A

Before 2 wks
>360 umol/L
BH4

26
Q

Tyrosinemia

A

Increased Tyr in the blood.

27
Q

Which tyrosinemia is most common and what is teh treatment?

A

Type I

Liver transplant

28
Q

Alkaptonuria

A

AKA black urine disease
Caused by accumulation of homogentisate
Noted also by black pigmentation in the IV disks
Auto recessive

29
Q

Which AA must be supplemented in a patient with PKU?

A

Tyr

30
Q

Ammonia toxicity

A

Excessive NH3

Causes pH imbalance, swelling in the brain

31
Q

Ammonia can cause a depletion of what?

A

Glutamate, an NT in the brain

32
Q

Gout

A

Build up of uric acid in the joints due to diets rich in purnies.

33
Q

Treatment of gout

A

Colchicine, which decreases movement of granulocytes to the affected area.
Allopurinol, which inhibits xanthine oxidase

34
Q

Altered uric acid excretion can come from (3):

A

Poor glomerular filtration, decreased tubular secretion or enhanced tubular resorption.

35
Q

Purine rich foods (6):

A

Beans, spinach, lentils, alcohol, meat and seafood.

36
Q

Hyperammonemia

A

Occurs in defects in any of the 6 enzymes in the urea cycle or with 3 transporters.

37
Q

Carbamoyl phosphate synthetase II function

A

First step in de novo synthesis of pyrimidines

38
Q

CPSaseI isoform chart (3)

A

Urea cycle
Mitochondrial
NAG-activated

39
Q

CPSaseII isoform chart (3)

A

Pyrimidine synthesis
Cytosolic
PRPP-activated

40
Q

Conjugated (direct) vs. unconjugated (indirect) bilirubin

A

Conjugated is soluble

Unconjugated is not soluble

41
Q

Jaundice in newborns is due to:

A

Build up of unconjugated bilirubin as the baby’s liver is not matured enough to process.
Should return to normal 7-10 days after delivery

42
Q

Physiological jaundice

A

Jaundice due to adult pathology - sickle cell, liver diseae, anemias, etc.

Renal Exam #1 (9 decks)

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