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nutritional aspects of disease > exam 3/final exam > Flashcards

exam 3/final exam Flashcards

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1
Q

What percent of bone cells are living? What percent are non-living?

A

2-5% are Living

95-98% are Non-Living, mineral encrusted protein-matrix (osteoid)

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2
Q

What is osteoid?

A

the mineral encrusted protein- matrix of nonliving material in bone

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3
Q

What are osteocytes?

A

they are master regulators that have processes that come out of their cell bodies

They reside in the matrix lacunae(space) and communicate through cellular processes

The canaliculi are microscopic canals of the osteocyte lacunae

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4
Q

70% of total bone is what?

A

carbonate hydroxyapatite

Calcium, phosphate and carbonate

40% of bone weight is calcium

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5
Q

the protein matrix consists of what percent collagen?

A

90%

Collagen is a single strand triple coil building mineral content on top of each other

10% is noncollagenous organic matrix

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6
Q

What are the four types of bone cells?

A

lining cells
osteoblasts
osteoclasts
osteocytes

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7
Q

osteoporosis is characterized by what?

A

decreasing mineral content on bones and getting weaker

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8
Q

Osteocytes do what?

A

they are master regulator cells that communicate other functions of other cell types (osteoblasts and osteoclasts)

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9
Q

Osteoblasts differentiate from osteoclasts how?

A

osteoblasts Build up minderal content (downregulated as you age but still functions)

Osteoclasts demineralize and break down mineral content

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10
Q

what do lining cells do?

A

they provide barriers of bone

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11
Q

What are inborn errors of metabolism?

A

large group of rare disorders caused by inherited deficiency or absence of proteins that have enzymatic, carrier, receptor or structural roles

For many, the molecular nature of the disorder is known

Responds to nutrient therapy intervention

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12
Q

Those most frequently identified disorders are those in which the absent or defective protein does what?

A

serve an enzymatic function

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13
Q

What are some examples of inborn errors of metabolism?

A 
phenylketonuria
Galactosemia
Glycogen Storage disease
homocystinuria
Maple syrup urine disease
branched chain ketoaciduria
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14
Q

In mutant DNA, what happens to the protein?

A

defects in structure/activity of protein, block normal flow of metabolic processes

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15
Q

what is the pathophysiology of inborn errors of metabolism?

A

accumulation, deficiency or overproduction of normally occurring substrates and products of metabolic flow

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16
Q

What is the diagnosis for inborn errors of metabolism?

A

symptoms presented by infants, lab analysis confirms biochemical and DNA analysis

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17
Q

What is the treatment for inborn errors of metabolism?

A

nutritional intervention modifies components of diet to correct the metabolic imbalance

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18
Q

What happens when you modify the components of diet to correct the metabolic imbalance?

A

you decrease the substrate available for the reaction, supplement the product to normal level, and enhance the enzyme activity by supplying its co-factor

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19
Q

What are the three assessments done in nutritional assessment and monitoring?

A

growth
nutrient intake
biochemical paramters

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20
Q

Why is there a variable outcome when treating inborn errors of metabolism?

A

depends on early diagnosis and intensive and continuous intervention

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21
Q

what alleviates toxic manifestations in inborn errors of metabolism?

A

modification of the dietary supply

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22
Q

What prevents poor outcome in the clinical characteristics of inborn errors of metabolism?

A

early diagnosis and early treatment

irreversible damages could occur if you do not

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23
Q

What is phenylketonuria (PKU)?

A

group of inherited autosomal recessive disorders of phenylalanine metabolism associated with impaired ability to convert phenylalanine to tyrosine

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24
Q

What are the causes of PKU?

A

inherited defects in :

phenylalanine hydroxylase (PAH) which is classic PKU

dihyydrobiopterin reductase (DHPR)
dhydrobiopterin biosynthesis
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25
What is the pathogenesis of PKU
>deficiency of Tyr causes CNS damage >deficient myelination (non treated causes are impaired brain development and irreversible) >abnormalities in brain proteolipids and/or proteins >depressed protein synthesis >imbalance in intraneuronal amino acid concentration
26
when does pku express itself in children?
3 months of age developmental delay, abnormal electroencephalogram, musty odor
27
What is the blood phenylalaline level?
>2 mg/dL`
28
What is the diagnosis for pku?
plasma aa anaylsis dna diagnosis family history prenatal diagnosis genotyping of parents, carrier detection
29
Treatment of PKU?
maintain blood Phe to prevent CNS damage restricted diet start as soon as diagnosis is established within 3 weeks of age optimal blood phe is 60-300 µmol/L tyrosine supplement adequate energy, protein and other nutrients
30
What is galactosemia?
a group of inherited autosomal recessive disorders of galactose metabolism
31
What are the causes of galactosemia?
defects in three enzymes 1. Galactose 1-phosphate-uridyl transferase (GALT) 2. galactokinase 3. 4-epimerase
32
What is the pathophysiology of GALT deficiency?
accumulation of Gal-1-P --> reduce ATP, GTP, and CTP inhibit galactation of phospholipids UPD-Gal deficiency, accumulation of galactose and its byproducts affect intracellular osmolality
33
What are symptoms of gal-1-p (gal-1-puridyltransferase)?
``` classic galactosemia (cataracts, growth failure, mental retardation, liver failure) ```
34
if both mom and dad are carriers of galactosemia, what is the percentage breakdown of acquiring the disorder?
50% carrier 25% galactosemia 25% neither
35
if galactosemia is untreated?
hepatoxicity (hyperbilirubinemia, hepatomegaly, cirrhosis) infection and sepsis: impaired immune infections kidney damages CNS damage: mental retardation growth failure Galactosemic infants given milk leave it unmetabolized and sugars build up to damage the liver, kidneys and brain
36
diagnosis of galactosemia?
newborn screening, biochemical analysis: GALT activity, GAL-1-P DNA analysis prenatal exam: GALT enzyme check
37
treatment of galactosemia?
prevent symptoms and support growth and development Galactose restricted diet Provide enough energy, protein and other nutrients
38
What is the galactose restricted diet?
AVOID ALL OF THESE: remove all sources of galactose and lactose from diet formula: soy milk ACCEPTABLE: fruits, cereals, legumes, nuts, and vegetables are acceptable
39
What is branched chain α-ketoaciduria (Maple syrup urine disorders)?
a group of hereditary autosomal recessive disorders of Ile, Leu, and Val metabolism, which is caused by imapired branched-chain α-ketoacid dehydrogenase
40
What is the incidence rate of α-ketoaciduria, galactosemia, and phenylketonuria?
α-ketoaciduria 1:180k galactosemia 1: 20k phenylketonuria . 1:15k
41
What are the clinical characteristics of α-ketoaciduria?
clinically normal until after eating dietary protein Increased BCKA and BCAA (branched achain amino acid) in blood, urine and cerebrospinal fluid fragrant urine with odor of maple syrup progressive neurological dysfunction: deficient myelination non-treated Maple Syrup Urine Disorder causes death (20%) or permanent neurological damage
42
Diagnosis of Maple syrup urine disorder aka branched chain ketoaciduria?
newborn screening leucine > 4mg/dL plasma and urinary val, leu, ile, and BCKA enzyme activity DNA analysis
43
treatment for branched chain ketoaciduria?
prevent accumulation of neurotoxic BCKAs maintain plasma BCAA at optimal level thiamin supplement: stabilize the enzyme complex high energy intake prevents protein catabolism
44
Von Gierke's Disease Type I glycogen storage disease details?
age of onset: newborn 3-4mo glucose-6-phosphatase enzyme deficiency: enzyme responsible for cleaving off PO4 from glucose liver and kidneys affected REQUIRED to obtain glucose to be released into circulation from liver glycogen and glucogenesis growth retardation, UNTREATED: hypoglycemia and hyperlipidemia
45
how to treat von gierke's Type I disease?
constant supply of carbs to prevent glucogenesis and lipolysis
46
calcium is a large nutrient reserve for which two minerals?
calcium in form of calcium homeostasis phosphorous depends on daily intake and excretion
47
bone mass depends on a variety of what nutrient factors?
genetics mechanical loading hormonal status
48
low bone mass always signifies reduced ____ reserve
calcium
49
difference between gp cartilage and articular cartilage
glycoproteins in gp cartilage and smooth white tissue covering ends of bones in articular cartilage
50
origin of osteoclasts
hemopoietic stem cell -> monocytes/monocyte lineage -> osteoclast multinucleated
51
origin of osteoblasts
stem cells > mesenchymal stem cells > pre-osteoblasts/osteoblasts/osteocytes
52
other names for cortical bone and trabecular bone are _____
cortical bone = compact bone | trabecular bone = spongy bone
53
why do weight bearing bones have different percentages in trabecular and cortical bone?
bone that bears more weight must be flexible Ex. ribcage is >75% trabecular spongy bone
54
What are the MAJOR nutrients influencing skeletal metabolism?
Ca, P, Vit D -- rickets, bone mineralization REtinoic Acid -- Limb development Cu -- cartilage dysplasia, collagen, cross-linking Zn -- dwarfism Other mineral deficiencies that can be associated with skeletal system deficiency
55
What are the MINOR nutrients influencing skeletal metabolism?
B, F, Sr -- osteoporosis, stimulate osteoblast activity Se -- skeletal growth Vitamin K - osteoporosis Ascorbic acid -- skeletal matrix, collagen
56
calcium contrasts with majority of other nutrients. How does this lead to disease?
other nutrients have reserves, which are depleted first with no impact on biochemical function after reserve is depleted, metabolic pool used is exhausted --> disease Calcium has VAST RESERVE and biochemical pathways not impaired but bone strength dependent on bone mass so DECREASE IN CALCIUM RESERVE IS DECREASE IN BONE STRENGTH
57
Why does reabsorbtion occur in the skeleton during menopause, anorexia nervosa, and athletic amenorrhea?
skeleton sense more bone than it needs for reabsorption occurs to greater extent than formation
58
regular menstruation is the key to calcium maintenance in who?
young women, but same phenomenon occurs in men when testosterone is lacking
59
when are bending setpoints of skeleton high and low?
level of gonadal hormones determinant high at puberty low at menopause
60
what does vitamin D do in relation to calcium?
promotes absorption of calcium, development of healthy bones and teeth
61
WHAT IS THE METABOLICALLY ACTIVE VITAMIN D?
dihydroxyvitamin D3 ^ calcium absorption in small intestine ^ urinary calcium re-absorption in kidney ^bone mineralisation MAINTAINS CALCIUM BALANCE IN THE BODY VIA THE ACTION OF PARATHYROID HORMONE
62
rickets occur from deficiency in what nutrients?
calcium and vit D
63
mass and density of bone affected by what three factors?
nutrition physical activity gonadal hormones
64
Osteoporosis is defined as what
condition of skeletal fragility due to decreased bone mass and to microarchitectural deterioration of bone tissue, with consequent increased risk of fracture, not a single disorder but a group of discrete fracture syndromes
65
what are causes of osteoporosis?
increased activity of osteoclasts in response to estrogen deficiency, decreased activity of osteoblasts and rate or trabecular and cortical bone resorbtion exceeds bone formation
66
minor factors contributing to osteoporosis
family history physical inactivity fair complexions inadequate calcium and vitamin D intake
67
*what happens when your bones sense downregulation in estrogen level?
hemopoietic stem cells increase in cell differentiation and transform into osteoclasts, and thus overall increasing osteoclast activity
68
TOP THREE INFLUENCING FACTORS IN DEVELOPMENT OF OSTEOPOROSIS
BONE DENSITY DECLINES nutrition (calcium, vit D, acid base balance) Hormonal (growth hormone, estrogen, corticosteroids)
69
what is the difference in macronutrient intake and obesity over the years?
carb and fat intake increase with refined food fast food increase from 1970s to now liquid carbs poor compensation with solid carbs
70
what is difference in rats and humans for compensation?
misrepresent and overeat in form of beverage versus rats, who do sense the calories and stop eating
71
the research on rats -- procedure for calorie comepnsation
Performed hippocampal memory tests only after he stopped giving them Gave rats the beverages ony during teenage years of three weeks and stopped when they became adults Didn’t gain anymore weight and performed poorer Take home message: maintenance or overconsumption of beverages causes impairments in cognitive functions later in life Actual human children maintained on these drinks have impairments in cognitive function Giving them the beverage as adults had no affect but does in adolescence development it does
72
the western diet consumption and cognitive impairment has links to what?
hippocampal dysfunction and obesity
73
percentage breakdown of artificial sweeteners
``` aspartame -- 55 sucralose -- 13 acesulfame k -- 12 cyclamate --11 sacchasin -- 8 stevia -- 1 ```
74
most sweeteners a combo of which two sweeteners?
aspartame and ace k
75
saccharin is 300-500 x sweeter than sugar per gram but what are its other qualities
no food energy and not digested, passes through body unchanged OLDEST and tastes most artificial
76
aspartame is 200 x sweeter than sugar and provides how much energy
4 kcal energy per gram, limitations include short shelf life and not stable with eating gives energy bc it is an amino acid
77
ace k commonly combined with aspartame or sucralose in beverages and also 200x sweeter than sugar but what other qualities
not metabolized, excreted unchanged
78
sucralose 800x sweeter than sucrose but other qualities are
stable under heat not accidental discovery; made from sugar and substitutes 3 hydroxyl groups with chlorine: safe bc chlorine does not separate from sucralose
79
weight gain or loss from consuming artifical sweetened beverages
greater risk of weight gain and increased bmi CORRELATION NOT NECESSARILY CAUSALITY Association of weight gain Increase in ingestion of beverages and sweeteners went up over the years Increase in frequency of obesity no CONSISTENT evidence that ASB intake is associated with weight loss or gain in human popoulations
80
cck satiation signals
accumulation of chemical inhibitory signals that eventually causes satiety within the meal for meal termination, largely arising form the GI tract. Meal initiation is primarily the result of an absence of satiating signals.
81
liraglutide and exendin
rgalutide only drug approved to treat obesity, exendin treats diabetes liraglutide meets 5-10% sustained weight loss but exendin does not. *liraglutide meets it but plateaus

nutritional aspects of disease (3 decks)

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