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Flashcards in functional med november Deck (145)
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1

1. What types of biochemical perturbations/lesions are predisposing and propagating factors involved in the etiology of chronic diseases?

a. Amino acid substitutions or deletions in protein primary structures - changes in higher order protein structures that affect structure and function - change cell architecture or enzyme activities. B. Toxicant may cause alterations in cell structural components or they may bind to enzyme active sites, blocking required biochemical pathways.

2

2. How does early detection of nutrient deficiency prevent chronic degenerative disease?

a. Early detection can lead to interventions that restore nutrient levels to values that enhance the recovery of normal cellular and tissue function.

3

3. How do standard therapeutic interventions for heart disease or depression affect a patient’s nutritional status?

a. Use of drugs like statins for atherosclerotic heart disease or SSRIs for depression serve to avert the short term effects of the disease, but they can exacerbate underlying nutrient insufficiencies or toxic effects.

4

4. As of 2001 (the year of publication for reference 317 of Chapter 4), how many genetic mutations of PAH were known to cause some variant of PKU?

In what enzyme? phenylalanine _________

a. 400, phenylalanine hydroxylase

5

5. What other enzyme is a principal cause of PKU?
hint _ _ _ cyclohydrolase

What is the biochemical relationship of this enzyme to the clearance of excess L-phenylalanine?

a. GTP cyclohydrolase

can have mutations that decrease the available levels of BH4 (Tetrahydrobiopterin)that is required as a coenzyme for Pulmonary hypertension (PAH)

6

6. For enzymes with vitamin-derived cofactor requirements, is there any difference between the clinical outcome from a genetic alteration in the protein structure and dietary deficiency of the nutrient required for production of the cofactor?

a. No.

Differences in manifestations arise the age of onset and severity of outcome from strongly disrupting genetic mutations.

7

(CI 2.1) Why is it unusual to find elevated lipid peroxides when fat-soluble vitamins in serum are in their upper ranges? What does such a finding tell you about other nutrients that need evaluation?

• (CI 2.1) an indication that an individual has normal levels of protection against oxidative stress
- because many of the primary antioxidant functions are carried out by those vitamins, especially regarding biological membrane damage revealed by elevated lipid peroxides.
-The pattern found suggests that there may be elevated levels of membrane components that are easily oxidized, principally the polyunsaturated fatty acids.

8

(CI 2.2) Which vitamin insufficiencies are indicated by elevated branched chain keto acids in urine?

B1, B2, B3, folate and lipoic acid
B1, B2, B3, B5 and lipoic acid
B1, B2, B3, B12 and lipoic acid
B1, B2, B3, B6 and lipoic acid

• (CI 2.2) Elevated BCKA indicates low activity for the BCKA dehydrogenase complex that can be caused by deficiencies for one of its 5 B-vitamin-derived coenzymes, B1, B2, B3, B5 and lipoic acid.

9

(CI 2.3) How does urinary formiminoglutamate testing add clinical insight to homocysteine testing?

• (CI 2.3) Elevated HCys can be due to several factors, one of which is folate deficiency. Finding a normal level of FIGLU helps to rule that out as a cause.

10

What organ failure most directly causes multiple low essential trace elements to be found in blood or urine? Why do such patients frequently show only slowly improving trace element status?
r

• (CI 3.1) Failure of hydrochloric acid output by the stomach reduced the digestion of dietary protein and the accompanying release of bound multivalent elements. Supplementing the elements without correcting the stomach acid deficiency may be poorly effective because (1) foods are the major source of daily element intake and (2) lack of properly timed pH shifts can interfere with the sequence of events required fodelivering added elemental salts to absorptive surfaces in the small intestine. Free amino acids and small peptides from dietary protein are often required intermediate ligands for element absorption.

11

If you are called to review the records of a patient who has undergone multiple heavy metal detoxification procedures, what change in treatment is suspected when previously normal urinary mercury suddenly shows strong elevation?

• (CI 3.2) Rapid increase in Hg found in body fluids when no significant change in exposure has occurred could be due to either physician-guided chelation therapy or patient-administered forms of chelating agents such as sulfur amino acid that can mobilize Hg from deep sequestered sites such as bone.

12

What amino acid evaluation would come to mind for a patient with chronic thyroid insufficiency?

• Low tyrosine and phenylalanine

13

(pp 188-189) What effect does delayed specimen transport have on relative levels of glutamate (glu) and glutamine (gln)?

• (pp 188-189) Spontaneous hydrolysis of the amide side chain causes Gln conversion to Glu in specimens that are either delayed or warmed during transit.

14

(pp 222-230) The reciprocal regulation of transmethylation and transulfuration of HCys shown in Fig. 4.20 translates to decreased availability of HCys for reformation of Met.

What pattern of amino acids in plasma might indicate chronic presence of such effects in a patient?

why would this happen?


The reciprocal regulation of transmethylation and transulfuration of HCys shown in Fig. 4.20 translates to decreased availability of HCys for reformation of Met as shown in Fig. 2.11. The reduced flow of Met tends to reduce available active methyl (S-adnosylmethionine) for all methylation reactions shown in Fig. 2.11. Multiple clinical outcomes can be associated with these competing demands for homocysteine.

15

What body function uses the most amount of AA's?

Protein synthesis is, by far, the greatest demand on absorbed amino acids, far outpacing other products such as neurotransmitters or hormones like thyroxin.

16

A consequence of this fact (Protein synthesis is, by far, the greatest demand on absorbed amino acids) is that patients who show dramatic responses to therapies of customized essential amino acids are most likely demonstrating clinical effects of ____ ____ ____.

This is especially true regarding the organs with greatest turnover rates like the __1__ and _2_. In the _2_, the only process that can approach the magnitude of amino acid demand for protein synthesis is glutathione synthesis in a patient under chronic, severe oxidative or toxicant stress.

restored organ reserve

GI tract and liver

17

(Fig 4.11) What compound is abbreviated “ADMA.” What cell regulator does elevated levels of ADMA in blood affect? What symptom is frequently produced?

ADMA stands for assymetric dimethylarginine

it inhibits nitric oxide synthase, regulating the multiple, powerful effects of that cell regulator.

Excessive ADMA frequently produces hypertension due to lack of NO to induce vasodilatation.

18

(Fig 4.17) What elemental cofactor is required for conversion of dopamine to norepinephrine? For what enzyme?

And what vitamin derivative?

• (Fig 4.17) Copper ions are a critical cofactors required by dopamine hydroxylase.

also needs ascorbate

19

why does finding a pattern of strongly elevated serine with low glycine on a plasma amino acid profile may be related to patient symptoms of poor growth, maldigestion, impaired cognition or excessive fatigue?

-Gly and Ser are related by a single reaction that transfers the hydroxymethyl group,
-they normally move up and down together on amino acid profiles.
-When they do not, then other pathway interferences are suspected, mainly glycine cleavage system
- genetic or toxicant interruption of that enzyme would tend to prevent the degradation of glycine.
-The resulting accumulation of glycine would tend to reduce activity of the Gly to Ser conversion, leading to such a pattern of elevated Gly and normal or low Ser.

-Since that pathway is a major source of single carbon for the THF pathways (Fig 2.11), multiple biosynthetic and methylation defect manifestations may be found.

20

finding a pattern of strongly elevated serine with low glycine on a plasma amino acid profile, Which micronutrients are potential causes or confounding factors?

That system may be activated by added vitamin B6 or folate.

21

finding a pattern of strongly elevated serine with low glycine on a plasma amino acid profile, : If your assessments indicate normal levels of those micronutrients (B6 or folate), what other explanation is likely for the amino acid abnormality pattern?

If various evaluations indicate normal levels of those vitamins, then a genetic polymorphism in the glycine cleavage system enzyme is indicated, as occurs in the condition known as non-ketotic hyperglycinemia.

22

finding a pattern of strongly elevated serine with low glycine on a plasma amino acid profile: What further information about health effects related to the pattern is suggested by the information in Fig. 4.23?

• (Fig’s 4.22 and 4.23). Since that pathway is a major source of single carbon for the THF pathways (Fig 2.11), multiple biosynthetic and methylation defect manifestations may be found.

23

Describe a typical procedure for producing a customized free-form amino acid product.

• (Fig 4.30b) performing a plasma amino acid profile and using the results to produce an essential amino acid mixture where the degrees of low levels in plasma govern amounts added for each amino acid. The usual dosing of the product for adults is a rounded teaspoon twice daily.

24

(CI 4.3) What amino acid imbalance is indicative of ornithine transcarbamylase deficiency? Why?

• (CI 4.3) Genetic polymorphisms in any of the four enzymes of the urea cycle tend to produce strong elevations of urea cycle intermediate products measured in profiles of plasma amino acids. In the case of OTC deficiency, the greatest elevation is usually in its substrate, ornithine.

pg 201 -

25

Antidepressants can deplete

• B vitamins, Se, Zn, GSH, Ca, Mg, Vit C
• Low plasma AA
• AA’s, Cu, mercury toxicity, lithium def. low cholesterol, low GABA
• Mg, Tauu, Vitamin E
• B vitamins, low plasma AA
• Arg, Arsenic, beta carotene, Iodine, Niacin, Se, Strontium, Vitamin C, zinc

B vitamins, Se, Zn, GSH, Ca, Mg, Vit C

26

Diabetes can cause what Nutrient Def?

• B vitamins, Se, Zn, GSH, Ca, Mg, Vit C
• Low plasma AA
• AA’s, Cu, mercury toxicity, lithium def. low cholesterol, low GABA
• Mg, Tauu, Vitamin E
• B vitamins, low plasma AA
• Arg, Arsenic, beta carotene, Iodine, Niacin, Se, Strontium, Vitamin C, zinc


Mg, Tauu, Vitamin E

27

Heart disease can be related to what nutrient def.

• B vitamins, Se, Zn, GSH, Ca, Mg, Vit C
• Low plasma AA
• AA’s, Cu, mercury toxicity, lithium def. low cholesterol, low GABA
• Mg, Tauu, Vitamin E
• B vitamins, low plasma AA
• Arg, Arsenic, beta carotene, Iodine, Niacin, Se, Strontium, Vitamin C, zinc
• oxidative stress, nutrient def. insufficiency of antioxidants, toxicity. Arginine, niacin, CoQ10, vitamin C, E, B vitamins


(not listed in book)--oxidative stress, nutrient def. insufficiency of antioxidants, toxicity. Arginine, niacin, CoQ10, vitamin C, E, B vitamins

28

Cancer related nutrient def.

• B vitamins, Se, Zn, GSH, Ca, Mg, Vit C
• Low plasma AA
• AA’s, Cu, mercury toxicity, lithium def. low cholesterol, low GABA
• Mg, Tauu, Vitamin E
• B vitamins, low plasma AA
• Arg, Arsenic, beta carotene, Iodine, Niacin, Se, Strontium, Vitamin C, zinc



arginine, arsenic toxicity, beta carotene, iodine, niacin, selenium, strontium, vit C, zinc

29

Chronic fatigue related nutrient def.

• B vitamins, Se, Zn, GSH, Ca, Mg, Vit C
• Low plasma AA
• AA’s, Cu, mercury toxicity, lithium def. low cholesterol, low GABA
• Mg, Tauu, Vitamin E
• B vitamins, low plasma AA
• Arg, Arsenic, beta carotene, Iodine, Niacin, Se, Strontium, Vitamin C, zinc


Low plasma AA

30

Depression related nutrient def.

• B vitamins, Se, Zn, GSH, Ca, Mg, Vit C
• Low plasma AA
• AA’s, Cu, mercury toxicity, lithium def. low cholesterol, low GABA
• Mg, Tauu, Vitamin E
• B vitamins, low plasma AA
• Arg, Arsenic, beta carotene, Iodine, Niacin, Se, Strontium, Vitamin C, zinc

B vitamins, low plasma AA