Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

exam 3/final exam Flashcards

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is osteoid?

A

the mineral encrusted protein- matrix of nonliving material in bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

70% of total bone is what?

A

carbonate hydroxyapatite

Calcium, phosphate and carbonate

40% of bone weight is calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the four types of bone cells?

A

lining cells
osteoblasts
osteoclasts
osteocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

osteoporosis is characterized by what?

A

decreasing mineral content on bones and getting weaker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Osteocytes do what?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what do lining cells do?

A

they provide barriers of bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

serve an enzymatic function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

In mutant DNA, what happens to the protein?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the diagnosis for inborn errors of metabolism?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the treatment for inborn errors of metabolism?

A

nutritional intervention modifies components of diet to correct the metabolic imbalance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

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

A

growth
nutrient intake
biochemical paramters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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

A

depends on early diagnosis and intensive and continuous intervention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what alleviates toxic manifestations in inborn errors of metabolism?

A

modification of the dietary supply

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the causes of PKU?

A

inherited defects in :

phenylalanine hydroxylase (PAH) which is classic PKU

dihyydrobiopterin reductase (DHPR)
dhydrobiopterin biosynthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the pathogenesis of PKU

A

> 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

when does pku express itself in children?

A

3 months of age

developmental delay, abnormal electroencephalogram, musty odor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the blood phenylalaline level?

A

> 2 mg/dL`

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the diagnosis for pku?

A

plasma aa anaylsis
dna diagnosis
family history prenatal diagnosis
genotyping of parents, carrier detection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Treatment of PKU?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is galactosemia?

A

a group of inherited autosomal recessive disorders of galactose metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the causes of galactosemia?

A

defects in three enzymes

  1. Galactose 1-phosphate-uridyl transferase (GALT)
  2. galactokinase
  3. 4-epimerase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the pathophysiology of GALT deficiency?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are symptoms of gal-1-p (gal-1-puridyltransferase)?

A 
classic  galactosemia
(cataracts, growth failure, mental retardation, liver failure)
34
Q

if both mom and dad are carriers of galactosemia, what is the percentage breakdown of acquiring the disorder?

A

50% carrier
25% galactosemia
25% neither

35
Q

if galactosemia is untreated?

A

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
Q

diagnosis of galactosemia?

A

newborn screening,
biochemical analysis: GALT activity, GAL-1-P
DNA analysis
prenatal exam: GALT enzyme check

37
Q

treatment of galactosemia?

A

prevent symptoms and support growth and development
Galactose restricted diet
Provide enough energy, protein and other nutrients

38
Q

What is the galactose restricted diet?

A

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
Q

What is branched chain α-ketoaciduria (Maple syrup urine disorders)?

A

a group of hereditary autosomal recessive disorders of Ile, Leu, and Val metabolism, which is caused by imapired branched-chain α-ketoacid dehydrogenase

40
Q

What is the incidence rate of α-ketoaciduria, galactosemia, and phenylketonuria?

A

α-ketoaciduria 1:180k galactosemia 1: 20k phenylketonuria . 1:15k

41
Q

What are the clinical characteristics of α-ketoaciduria?

A

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
Q

Diagnosis of Maple syrup urine disorder aka branched chain ketoaciduria?

A

newborn screening leucine > 4mg/dL
plasma and urinary val, leu, ile, and BCKA
enzyme activity
DNA analysis

43
Q

treatment for branched chain ketoaciduria?

A

prevent accumulation of neurotoxic BCKAs

maintain plasma BCAA at optimal level
thiamin supplement: stabilize the enzyme complex
high energy intake prevents protein catabolism

44
Q

Von Gierke’s Disease Type I

glycogen storage disease details?

A

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
Q

how to treat von gierke’s Type I disease?

A

constant supply of carbs to prevent glucogenesis and lipolysis

46
Q

calcium is a large nutrient reserve for which two minerals?

A

calcium in form of calcium homeostasis
phosphorous

depends on daily intake and excretion

47
Q

bone mass depends on a variety of what nutrient factors?

A

genetics
mechanical loading
hormonal status

48
Q

low bone mass always signifies reduced ____ reserve

A

calcium

49
Q

difference between gp cartilage and articular cartilage

A

glycoproteins in gp cartilage and smooth white tissue covering ends of bones in articular cartilage

50
Q

origin of osteoclasts

A

hemopoietic stem cell -> monocytes/monocyte lineage -> osteoclast multinucleated

51
Q

origin of osteoblasts

A

stem cells > mesenchymal stem cells > pre-osteoblasts/osteoblasts/osteocytes

52
Q

other names for cortical bone and trabecular bone are _____

A

cortical bone = compact bone

trabecular bone = spongy bone

53
Q

why do weight bearing bones have different percentages in trabecular and cortical bone?

A

bone that bears more weight must be flexible

Ex. ribcage is >75% trabecular spongy bone

54
Q

What are the MAJOR nutrients influencing skeletal metabolism?

A

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
Q

What are the MINOR nutrients influencing skeletal metabolism?

A

B, F, Sr – osteoporosis, stimulate osteoblast activity
Se – skeletal growth
Vitamin K - osteoporosis
Ascorbic acid – skeletal matrix, collagen

56
Q

calcium contrasts with majority of other nutrients. How does this lead to disease?

A

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
Q

Why does reabsorbtion occur in the skeleton during menopause, anorexia nervosa, and athletic amenorrhea?

A

skeleton sense more bone than it needs for reabsorption occurs to greater extent than formation

58
Q

regular menstruation is the key to calcium maintenance in who?

A

young women, but same phenomenon occurs in men when testosterone is lacking

59
Q

when are bending setpoints of skeleton high and low?

A

level of gonadal hormones determinant

high at puberty
low at menopause

60
Q

what does vitamin D do in relation to calcium?

A

promotes absorption of calcium, development of healthy bones and teeth

61
Q

WHAT IS THE METABOLICALLY ACTIVE VITAMIN D?

A

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
Q

rickets occur from deficiency in what nutrients?

A

calcium and vit D

63
Q

mass and density of bone affected by what three factors?

A

nutrition
physical activity
gonadal hormones

64
Q

Osteoporosis is defined as what

A

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
Q

what are causes of osteoporosis?

A

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
Q

minor factors contributing to osteoporosis

A

family history
physical inactivity
fair complexions
inadequate calcium and vitamin D intake

67
Q

*what happens when your bones sense downregulation in estrogen level?

A

hemopoietic stem cells increase in cell differentiation and transform into osteoclasts, and thus overall increasing osteoclast activity

68
Q

TOP THREE INFLUENCING FACTORS IN DEVELOPMENT OF OSTEOPOROSIS

A

BONE DENSITY DECLINES

nutrition (calcium, vit D, acid base balance)
Hormonal (growth hormone, estrogen, corticosteroids)

69
Q

what is the difference in macronutrient intake and obesity over the years?

A

carb and fat intake increase with refined food fast food increase from 1970s to now

liquid carbs poor compensation with solid carbs

70
Q

what is difference in rats and humans for compensation?

A

misrepresent and overeat in form of beverage versus rats, who do sense the calories and stop eating

71
Q

the research on rats – procedure for calorie comepnsation

A

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
Q

the western diet consumption and cognitive impairment has links to what?

A

hippocampal dysfunction and obesity

73
Q

percentage breakdown of artificial sweeteners

A 
aspartame -- 55
sucralose -- 13
acesulfame k -- 12
cyclamate --11
sacchasin -- 8
stevia -- 1
74
Q

most sweeteners a combo of which two sweeteners?

A

aspartame and ace k

75
Q

saccharin is 300-500 x sweeter than sugar per gram but what are its other qualities

A

no food energy and not digested, passes through body unchanged

OLDEST and tastes most artificial

76
Q

aspartame is 200 x sweeter than sugar and provides how much energy

A

4 kcal energy per gram, limitations include short shelf life and not stable with eating

gives energy bc it is an amino acid

77
Q

ace k commonly combined with aspartame or sucralose in beverages and also 200x sweeter than sugar but what other qualities

A

not metabolized, excreted unchanged

78
Q

sucralose 800x sweeter than sucrose but other qualities are

A

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
Q

weight gain or loss from consuming artifical sweetened beverages

A

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
Q

cck satiation signals

A

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
Q

liraglutide and exendin

A

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions