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Biochem 1502 > Winter Exam 4 > Flashcards

Winter Exam 4 Flashcards

1
Q

What is marasmus?

A

Adaptive response to chronic under-nutrition
‘simple starvation’ from successful adaptation
cathetic (emaciated)
normal albumin levels
immune function preserved

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2
Q

What is kwashiokor?

A 
Pathological rapid response with high mortality
decreased protein intake (stress)
edema
ABnormal albumin levels
immune function compromised
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3
Q

What is Protein energy malnutrition?

A

Low caloric and Low protein intake

accompanied by micronutrient deficiencies

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4
Q

Which patients are most at risk fro develping malnurtition?

A
  • feeding tubes/nutrition supplements
  • low income
  • GI disease limiting absorption
  • alcohol/drugs
  • cancer
  • ELDERLY
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5
Q

Why are elderly patients at high risk for malnutition?

A 
Depression
Meds
GI tract aging
lower sense of taste
B12 deficiency
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6
Q

Which type of test can help determine the type of malnutrition occuring?

A

serum albumin test
3.5-5 is normal
<2.1 is severely malnourished

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7
Q

What are the ABCDs of nutrition classification?

A

Anthropometric
Biochem lab tests
Clinical Signs
Diet History

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8
Q

What are some anthropometric measures?

A

Weight
BMI
Skin fold thickness
Arm circumference

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9
Q

What non-nutritional factors can effect albumin levels?

A

Injury/disease
Kidney disease
Liver disease (cirrhosis)
Dehydration status

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10
Q

How will injury and disease affect albumin levels?

A

acute phase resopnse
C reactive protein produced
For this, albumin must be downgraded
Low albumin level = negative response

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11
Q

How does albumin’s half life (21 days) influence its usefulness as a marker for nutritional status?

A

long term marker

not a day-to-day basis

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12
Q

What markers can you use on a short term basis for nutritional status?

A 
serum transferrin
free albumin (this is not albumin)
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13
Q

Describe acute metablic adaptations to starcation

A

Decrease in muscle mass
ketones
alanine for gluconeogenesis
Glucose to the brain

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14
Q

describe chronic metabolic adaptations to starvation

A

break down of stored fat
reduced alanine and glutamine
Ketones to the brain !

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15
Q

What is refeeding syndrome characterized by?

A

hypophosphatemia
hypokalemia
hypomagnesemia

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16
Q

What is the biochemical basis for hypophosphatemia dev.?

A 
increased metabolism -> increased ATP production
increased hexokinase (glycolysis)
increased need for PO4 from refeeding
this comes from extracellular
slow refeeding maintains homeostasis
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17
Q

Which nutrients are needed for Hb sunthesis?

A

B12, folate, iron

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18
Q

What is the creatine-height index?

A

measure rebuilding of muscle mass

muscle mass/lean body mass

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19
Q

During refeeding, what is the pattern of Reticulocyte index in relationship to creatin-height index?

A

RC index changes after creating-height index becuase an increase in muscle mass incraeased the need for 02

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20
Q

What problems are associated with obesity?

A 
Metabolic syndrome
DM
CV disease
HTN 
depression
stroke
apnea
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21
Q

What is the formula for BMI?

A

BMI = lbs / (in^2) X 703

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22
Q

What is the normal range of BMI?

A

18.5-24.9

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23
Q

How good of a marker is BMI a measurement for fat?

A

in children: good

in college kids: toss up, doesnt matter

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24
Q

What waist measurements indicate higher risk of disease in men and women?

A

men: <35 in

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25
Q

What is calipers?

A

measurement of subcutaneous fat

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26
Q

What is the heritability for BMI in adults and children?

A

~ 0.7

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27
Q

What gene is most strongly supported by evidence to be linked with obesity?

A

FTO
fat mass and obesity associated gene
involved in demethylation of nucleic acids

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28
Q

Where is the higheest concentration of FTO expressed?

A

hypothalamus

also adipocytes and nuclei

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29
Q

What is the risk allele for FTO associated with?

A

associated with decreased lipolysis in adipocytes

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30
Q

What are the allele forms of FTO?

A

AA: high risk of increased BMI
AT: middle risk
TT: low risk

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31
Q

What diseases can cause serum albumin to be decreased?

A

liver disease
kidney disease
poor nutrition
inflammation

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32
Q

On which FTO allele type does physical activity have the biggest impact>

A

AA

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33
Q

What can adipose tissue release as an endocrine organ?

A

adipokines
leptin etc.
high adipokines i nobesity

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34
Q

Describe leptin and its role in appetitie/energy expenditure

A

When eating, fat is stored in tissue
Then, leptin is released
Crosses BBB to bind to anorexogenic and orexogenc receptors in ARC (hypothalamus)
overeall effect: decrease appetite, increase E expenditure
(can also control fat deposition)

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35
Q

What does the stimulation of anorexogenic neurons release?

A

expression appetite inhibiting factors:
POMC
CART

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36
Q

What does the stimulatio nof orexogenic neurons release?

A

inhibition of of appetit stimulation factors:
Neuropeptide Y
AgRP

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37
Q

How is energy expenditure increased with lectin activity?

A

sympathetic nerve activity in brown adipose tissue to stimulate thermogenesis

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38
Q

Compare effects of leptin and insulin

A

both decrease appetite and increase E expenditure

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39
Q

What molecule help regulate appetite?

A 
leptin
insulin
ghrelin
cholecystokinin
glucose/lipids
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40
Q

What is the effect of leptin in skeletal muscles?

A

promotes insulin sensitivity

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41
Q

What is the relationshp bw leptin and AMPK?

A

Leptin stimulates AMPK -> phosphorylates regulatory enzymes ->
stimulates fatty acid biosynth

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42
Q

What is the rate limiting / commited step in fatty acid biosynth?

A

ACC enzyme
(acetyl coA -> malonyl coA)
ACC switched off when phosphorylated

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43
Q

If ACC is phosphoraylted, what happens?

A

ACC is inactivated
so decreased production of malonyl CoA
This stimulates CPT1

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44
Q

What does CPT1 do?

A

Transports fatty acids from cytosol to inner membrane (mitochondrial matrix) where fatty acids are oxidized

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45
Q

How are fatty acid oxidation and fat deposition related?

A

incerased oxidation leads to less deposition in skeletal muscle
decreases risk of DM2

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46
Q

What happens to leptin levels in obese patients?

A

Increased

because of leptin resistance, impaired signaling

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47
Q

What can exercise induced activation of AMPK lead to?

A

enhance mitochondrial biogenesis and

GLUT4 transporters in skeletal muscle

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48
Q

How does AMPK influence whole body energy metabolism?

A

Inhibits ATP anabolism (cholesterol, f.a. synth)
Promotes ATP catabolism (fatty acid oxidation)

also a nutrient sensor in fed and unfed state

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49
Q

How can metformin influence AMPK in different tissues?

A

Stimulates AMPK in liver and muscle

Inhibits AMPK in hypothalamus

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50
Q

What is the effect of metformin on the hypothalamus?

A

inhibits AMPK so decreases appetite

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51
Q

Decreases in leptin are associated with what changes in neuroendocrine function?

A

Decreased Thyroid hormone
Decreased IGF-1
Decreased Repro hormones
(all for lower E expenditure)

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52
Q

What can mutations (rare) in the leptin gene produce?

A

hyperphagia (excessive hunger)
obesity

leptin injection corrects this

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53
Q

What mechanism might enable leptin to assist in weight loss?

A

Weight loss decreases insulin and leptin resistance

Now, leptin can perform normal function of reducing appetite

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54
Q

What medical disorders are associated with acquired leptin deficiencies?

A

Eating disorders:

anorexia, bulemia

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55
Q

What are the sensitive periods of adipocyte dev. during growth?

A

1) 1st year of life - increase in volume (hypertrophy)

2) prior to puberty - increase in # (hyperplasia)

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56
Q

What are teh six categories of nutrients?

A 
carbs
lipis
proteins
vitamins
minerals 
water
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57
Q

What disease exhibits the highest death rate in our population?

A

heart disease

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58
Q

What does the Dietary Reference Intake include?

A

Estimated Average Req (EAR)
Recommended Dietary Allowance (RDA)
Adequate Intake (AI)
Tolerable Upper Intake Level (UL)

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59
Q

What are teh 3 essential energy uses?

A

basal metabolic needs
food intake effect
physical activities

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60
Q

What is the Estimated Average Requirement?

A

intake at which risk of inadequacy is 50%

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61
Q

What factors influence BMR?

A

lead body mass
growth
fever and disease
cold temps

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62
Q

How much does the BMR contribute to daily energy expenditure?

A

60-70%

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63
Q

Daily Value is absed on which dietary standards?

A

Daily Reference Values

Referenec Daily Intake

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64
Q

Which tissues are normally dependent on carbs?

A

brain
renal medulla
RBCs

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65
Q

What is the acceptable carb intake of carbs?

A

45-65% of caloric intake

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66
Q

Below what gram level of carbs can lead to problems? What kinds of problems?

A

Below 60g/day carbs

ketosis, tissue breakdown, cation loss (Na), dehydration

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67
Q

What are some water soluble fibers?

A

pectin
gums
mucilages
some hemicellulose

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68
Q

Wat are some water insoluble fibers?

A

cellulose
lignin
most hemicellulose

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69
Q

How do soluble and insooluble fibers benefit you?

A

soluble: daley emptying, lower cholesterol by binding bile acids (small intestines)
insoluble: accelerate emptying, dilutes fecal mutagens by increasing fecal weight (large intestines)

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70
Q

What are the AIs of fiber intake for men and women?

A

men: 38g/day
women: 25g/day

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71
Q

Which of the macronutrients are non-esential?

A

carbs

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72
Q

What are examples of disaccharadies?

A

lactose

maltose

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73
Q

What are some function of proteins?

A

builind and reparing tissues
purine, pyrimidine, heme snth
plasma protein synth (albumin)

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74
Q

What are essential amino acids? What are they?

A

required by body
but not produced by body - must be ingested
PVT TIM HALL

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75
Q

Where is protein turnover highes? lowest?

A

Highest? intestinal mucosa, liver, pancreas, kidney, plasma

Lowest: muscle, brain tissues

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76
Q

What is significant about muscle protein and amino acid reserve?

A

it is the only aminio acid reserve in body capable of significant losses without compormins the ability to sutain life
breakdown increases during fasted state

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77
Q

What is Nitrogen balance?

A

metabolic balance bw body;s intake and output of Nitrogen (dietary protein)

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78
Q

What is the ratio of protein consumption and N2 excretion?

A

for every 6.25g of protein consumed, 1g N2 excreted

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79
Q

What conditions will cause negative Nitrogen balance?

A

Greater N2 output than input:
inadequate dietary protein
lack of essential a.a.
metabolic stress

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80
Q

What conditions can cause positive nitrogen balance?

A

growth
pregnancy
lactation
recovery from metabolic stress

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81
Q

What a.a. deficiencies can be casued by exclusive eating of corn? wheat? beans?

A

corn: Trp , Lys
wheat: Lys
beans: Met

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82
Q

What percent of total energy supplied by protein is adquate?

A

12%

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83
Q

What are the main function of lipids and fats?

A

1) vehicle for fat soluble vitamins
2) to supply essential fatty acids that cant be synthesized by the body (linoleic, linolenic, arachidonic acid) (Omega 3 and 6s)

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84
Q

Which essential fatty acids are omega-6?

A

linolEIC acid

arachidonic acid

85
Q

What is the principal funciton fo essential fatty acids?

A 
precurosrs of local hormones:
leukotreines
prostoglandins
thromboxanes
(BUT ex: PGs from omega 3 varies from PGs of omega 6)
86
Q

What are exampels of dietary poly unsaturated fats? What are their benefits?

A

omega-6:
vegetable oils (corn, bean, sunflower)
Decrease plasma total and LDL-cholesterol

87
Q

What are some examples of monounsaturated fats?

A

olive and canola oils

Decrease plasma and total LDL cholesterol

88
Q

How can fish oils prevent CV diseases?

A 
omega 3s:
antiarrhytmia (major)
TAG lowering
HR lowering
BP lowering
Antithrombosis (minor)
89
Q

What are some antioxidants that can protect fats from goign rancid?

A

BHA
BHT
Vit C
Vit E

90
Q

What are the water soluble vitains?

A 
B1 - Thiamin
B2 - Riboflavin
B3 - Niacin
B6 - Pyridoxine
B12 - Cobalamins
Pathothenic acid
biotin
folate
Vit C
91
Q

Which of the wtaer soluble vitains can be stored inthe body?

A

B12 - Cobalamins

92
Q

What coenzyme is thiamin metabolized to? Where are its funcitons?

A

thiamin pyrophosphate

TCA cycle, glucose metab, nerve impulses

93
Q

What are varying severity of symptoms from thiamin (B1) deficiency?

A

moderate: in chronic alcoholics (wenicke korsakoff syndrome)

less severe: elderly

94
Q

What coenzyme is Riboflavin metabolized to? What are its functions?

A

FAD and FMN

redox

95
Q

What are symptoms of Riboflavin (B2) deficiencies?

A

angular cheilitis (mouth fissures)
glossitis
scaly dermatitis

96
Q

What coenzymes is Niacin (B3) metabolized to? Functions?

A

NAD+ and NADP+

redox

97
Q

Symptoms of Niacin (B3) deficincy?

A

pellagra
3Ds: dermatitis, diarrhea, dementia
moderate: lethargy, nervousness

98
Q

What can pharmological doses of Niacin do?

A

vasodilation
decreased mobilization of fattty acids from fat tissue
decreased cholesterol levels (LDL)
(this can help with hyperlipidemia)

99
Q

Which Vitamin defiecincies are related to alcoholics?

A

Thiamin
Riboflavin
Niacin
Folic acid

100
Q

What coenzyme is Pyrodoxine (B6) metabolized to? Fnctions?

A 
pyridoxal phosphate
catalyze (4):
transaminations
deaminations
decarboxulations
condensations
energy catabolisms, neuro, heme
101
Q

Which vitamin is responsible for the conversion of tryptophan to niacin?

A

pyridoxine (B6)

102
Q

What vitamin should women taking contraceptives take?

A

double dose of pyridoxine (B6)

103
Q

What coenzyme is pathothenic acid metaabolized to? Function?

A

CoA and phosphopantotheine

CoA for acyl transfers

104
Q

Which vitamin is not recognized with any diseases?

A

pantotheni acid

105
Q

What is the fucntion of biotin? Where is most of it produced

A

for carboxylation reactions (for glucose, f.a., succinyl CoA)
intestinal flora produces half of daily supply

106
Q

What food intake can lead to biotin deficiency?

A

raw egg whites

avidin protein binds biotin so tight that it cant be absorbed

107
Q

What is berberi?

A

neuromuscular symptoms
atrophy and wekaness of muscles
edema
heart failure

108
Q

What is sideroblastic anemia? When will you see it?

A

microcytic anemia in presence of adequate Fe

seen in B6 deficiency

109
Q

What are the hematopoietic vitamins? Why are they called so?

A

Vitamin B12 and folic acid

Because these deficiencies first efect hematopoiesis

110
Q

What are the two active forms of Vit B12

A

adenosyl cobalamin

methyl cobalamin

111
Q

What is the ingested form of B12?

OTC form?

A

ingested: hydroxy-cobalamin
OTC: cyano-cobalamin

112
Q

What is required for the absorption of B12?

A

Intrinsic factor, IF

Secreted by parietal cells

113
Q

What type of anemia is observed with B12 deficiency?

A

megaloblastic anemia (macrocytic)

114
Q

What is pernicious anemia?

A

inability ot utilize/absorb B12
lack of intrinsic factor from autoimmune rxn that destroys paietal cells
more common in elderly

115
Q

What may vegetarians be prone to?

A

B12 eficiency since plants have no B12

116
Q

Can plants or animals synthesize B12?

A

Neither can

absorption from bacteria that produces it in gut flora

117
Q

In nature, how many glutamic acid residues can folate contain?

A

7

118
Q

Which form of folate can humans absorb? Describe the process in the body

A

monoglutamate form of folate
conjugase (in brush border) hydrolyzes the poly form
transported to tissues
Then polyglutamated (ACTIVE coenzyme form)

119
Q

What must happen to polyglutamated folate in order to carry 1-carbon units?

A

Must be reduced to tetrahydrofolate form

120
Q

What is methotrexate?

A

a folic acid analogue used to treat:
psoriasis
RA
neoplasms

121
Q

Describe how B12 deficiency interferes with nucleic acid biosynth

A

“methyl folate trap” - methione synthase enzyme may be bad
Homocystein-> methion rxn is blocked
accumulation of methyl-FH4 and lack of FH4

122
Q

Which vitamin is the easist to become dificient?

What is the requirment?

A

Folic acid

400 microgams/day

123
Q

What can a lack of folate during pregnancy lead to?

A

Neural Tube Defects

124
Q

What is the coenzyme form of Vit C? Functions?

A 
ingested form
hydroxylation of prolyl and lysyl in collagen
iron absorption
antioxidant
prevents cataracts
125
Q

What may lower Vit C serum levels?

A

smoking
oral contraceptives
corticosteroids
Stress

126
Q

Which types of vitamin deficiencies are seen in microcytic, normocytic, and macrtocytic anemias?

A

micro: Fe, B6, Vit C
normo: protein/energy malnutrition
macro: B12, folate

127
Q

Which vitmain is invoved in heme biosynthese?

A

B6

128
Q

Which fat soluble vitamins are endogenously synthesized?

A

D (skin)

K (intestinal flora)

129
Q

Which fat soluble vitamins are converted to active forms in the body?

A

Vit A and D

130
Q

What is the most abudant caretonoid eaten by people?

A

B-carotene

131
Q

What family is Vitamin A a part of? Where do they come from?

A

VitA part of retinoids
Come from provitamins A (caretinoids)
1 caretnoid is cleaved into 2 VitA

132
Q

How much is 1 retinoid equivale equal to?

A

1 RE = 6 microg B-carotene and 12 microg of other caretinoids

133
Q

What form is dietary vitamin A mostly in?

A

retinyl esters in the fatty portions and

B-carotene from plants

134
Q

Whiat areas does Vitamin A functino in?

A

vision
gene regulation
antioxidant

135
Q

How do dietary retinyl esters eveentually end up in the liver or adipose tissue?

A

retinyl esters are hydrolyzed to retinol.
Retniol is transported into mucosal cells
Re-esterified and go into chylomicrons to liver

136
Q

How much supply can the liver store vitamin A?

A

6-12 months

137
Q

What proteins make up rhodopsin? What is its role in vision

A

opsin and 11-cis retinal

light induced conform. change of opsin produces nerve impulse mediated by cGMP

138
Q

Which form of vitamin A fnctions in gene regulation?

A

all-trans retinoic acid in epithelial cells

139
Q

What can occur from Vitamin A deficiencies?

A

keratin build up:

xerophtalmia - corneal keratinization

140
Q

How is active form of Vitamin D formed from sunlight?

A

7-dehydrocholesterol (skin) converted to cholecalciferol -> 25-OH-cholecalciferorl (liver) -> 1,25-diOH-cholecalciferol (kidney)

141
Q

What form is dietary vitamin D given in?

A

Vitamin D2 - ergocalciferol

142
Q

What is the funciton of the active form of Vitamin D (1,25-diOH-calciferol) ?

A

induces synthesis of protein for Ca absorption in intestinal cells
Acts with PTH to increase blood Ca levels (homeostasis)

143
Q

What can Vitamin D deficiencies cause in varying age populations?

A

children: rickets
adults: osteomalacia

144
Q

How many chemical form sare there for Vitamin E ?

A

8

145
Q

Which of the vitamin E chemical forms meets human requirements ?

A

alpha-tocopherol Vitmain E

146
Q

What is the main function of vitamin E?

A

antioxidant

147
Q

What is seen in hypovitmainosis in Vitamin E?

A

fragility of RBC membranes

148
Q

What is the main funcitno of Vitamin K?

A

cofactor in gamma carboxylation of glutamates in:
precoag. factors - 2, 7, 9, 10, C, S
bone proteins

149
Q

What are some preisponsing conditinos of Vit K deficiency (hemhorrage) ?

A

parenteral nutrition
malabsorption syndrome
liver dysfunction

150
Q

How much of alcohol is oxidized in liver?

A

80-90%

151
Q

What is the common product of the main pathways of alcohol metabolism?

A

acetaldehyde (very toxic)

152
Q

What are the 2 main pathwasy for alcohol metabolism?

A 
alcohol dehydrogenase (ADH) of cytosol (stomach, liver)
microsomal etahnol xoidizing system in ER (liver)
153
Q

How is first pass metabolism/gastric barrier lost in alcoholism?

A

decrease in gastric ADH activity from gastritis

154
Q

2 reasons why female alcohol blood levels are higher than males

A

higher fat content proportion

less gastric ADH activity, so more enters blood

155
Q

What is the most important metabolic effect of alcohol? What are other conditions?

A 
generation of NASH in liver- overwhelms liver
lactic acidosis
scondary hyperuricemia
TCA cycle depressed (NAD slowing)
hypoglycemia
fatty liver
156
Q

Where is the site for the adaptive system of ethanol oxisdaation (MEOS) ?

A

liver microsomes

157
Q

What types of enzymes oxidize alcohol?

A

cytochromeP450

-2E1

158
Q

Which enzyme is induced during chronic alcohol use?

A

2E1
This induction leads to metabolic tolerance EtOH
(Hepatic ADH is not inducible)

159
Q

Under what condition is P4502E1 most effective?

A

When large aounts of alcohol are consumed

160
Q

In which individulas is P4502E1 most effective?

A

alcoholics

161
Q

The enhanced metabolism of which drugs are seen in alcoholics?

A

analgesics (acetomenaphin, pentobarbital, cocaine)

162
Q

In the presence of high 2E1, tylenol is broken down to which toxic metaboliter?

A

NAPQ1

163
Q

Increase in P4502E1 may partially account for…

A

increased incidence of cancer in alcoholics
testicular atrophy
gynecomastia

164
Q

The effect of which enzyme is diminished with chronic alcoholism?

A

Aldehyde Dehydrogenase (ALDL)
diminshed activity leads to build up of acetylaldehyde
highly reactive via oxidative damage

165
Q

What is Ernicke-Korsakoff Syndomre?

A

severe thiamin deficiency
ataxia
ophthalmoplegia
mental confusion

166
Q

What is the cause of cirrhosis

A

toxic effect of alcohol and

malnutrition

167
Q

What is a potential treatment ofr alcoholism?

A

Disulfiram

conidtioned avoidance response to acetaldehyde build up

168
Q

When is stomach oxidation of alcohol decreased?

A

in alcoholics
in women
gastritis
drugs with alcohol

169
Q

Which minerals are essential micronutirents?

A 
Iron
Ca
Mg
An
Cu
Se
170
Q

Why is iron essential for life?

A

transport of compounds and oxygen

hemoglobin

171
Q

What are some heme proteins?

A

hemoglobin
myoglobin
various cytochromes

172
Q

What are some non0heme iron proteins?

A

Fe-S cluster proteins

173
Q

Where are teh 2 major storage sties of iron?

A

reticuloendothelial macrophages

liver

174
Q

What is transferrin?

A

transports iron between utilization and storgae sites

175
Q

how much iron does the body contain?

A

2-4 g

176
Q

Which iron form is quantitatvely more present? which is more biologically active?

A

quantitatively: non-heme
active: heme

177
Q

What are 3 observations of unique iron requirements?

A

Pregnancy requires more iron (27)
Postemenopausal requires less (8mg)
1st 6 months of life is very low requirement

178
Q

What is ferritin?

A

protein that sequesters iron and binds extra Fe

179
Q

What is the path of heme-Fe uptake in a cell?

A

heme -> HPC1-> HO -> then either stored or used

180
Q

What is ferroportin/IREG1?

A

transport protein that moves Fe out of cell

hepaestin (Cu) also needed for this

181
Q

What form is iron from a diet?

A

Fe 3+

182
Q

How can Fe 3+ be reduced to Fe2+ ?

A
  • Ferric Reductase (DytB) - brush border

- Vitamin C

183
Q

What are enhancers of absorption of iron?

A

VitC
citrate
meat factor
reducing sugars

184
Q

What are inhibitors of iron absorption?

A

phytates, calcium, tannates, carbs…

185
Q

What is iron homeostatsis regulated by?

A

hepcidin

  • synthesiezed in liver
  • prevents iron transport across gut and inhibits iron absorption when Fe levels are high
  • also traps iron inside macrophages
186
Q

How does hepcidin work?

A 
If liver signals an increase of iron:
more hepcidin is produced
interacts with ferroportin
gets degraded in enterocyte 'stuck'
Fe levels go back down
187
Q

What 3 proteins are involed in hepcidin regulation?

A

HFE, TFR2, HJV

188
Q

How will the hepcidin-ferroportin system be altered in iron defiecient patietns?

A

less iron in blood to interact with H-F complex
Hepcidin production will go down
Fe will be released from storage
and increased Fe absorption

189
Q

How will the hepcidin-ferroportin system be altered in infectous patients?

A

Since antimicrobial, hepcidin will be upregulated
also less Fe mobilization and less absorption
starves bad bacterioa of iron

190
Q

How will the hepcidin-ferroportin system be alteterd in a deleterious mutation of HFE gene?

A

Regulation is decreased
so decreaed expression of Hepcidin
storage will increase; absorption will increase

191
Q

Describe the 3 stages of iron deficiency?

A

1: Fe storage being depleted
2: impairment of erythropoeiss
3: overt iron deficient anemia

192
Q

What is the gold standard to test for iron storage?

A

stainable marrow iron

193
Q

What do serum ferritin levels indicate?

A

directly proportional to amount of iron stored

(But also increases with acute phase/inflammation

194
Q

What are the most commonly used test to test iron in erythroid tissues?

A 
serum iron
transferrin saturation (TSAT)
195
Q

Which test are most sensitive in changes to iron status?

A 
stainable marrow iron
serum iron (more practical)
196
Q

Which tests are elast sensitive to changes in iron status?

A

Hb, MCV, MCHC

197
Q

How do soluble transferrin receptor levels change with iron deficiency?

A

During deficiency, sTFr levels will increase
gene expression goes up
ferritin expression goes down

198
Q

Which subgroup is at higher risk for iron deficiency aemia?

A

pregnant women

199
Q

Describe anemia of chronic disease

A

cytokine mediated
in diseased patients
functional iron deficiency - adequate iron but cant go where it needs to
looks like iron deficiency but ferritin will be high

200
Q

Describe herediatry hemochromatosis

A

autosomal recessive
excess iron deposited in various tissues
most common type: HFE mutation

201
Q

What is the most abundant mineral in the body?

A

calcium

1000g

202
Q

What are normal serum calcium levels?

A

9-10 mg/dL

much of which is bound to albumin

203
Q

How will hypoalbuminia effect serum Ca levels?

A

total calcium levels iwll decrease proportionately

ionized Ca will remain same though

204
Q

What serum level determines hypo or hypercalcemia?

A

amoutn of ionized Ca

difficult to test though

205
Q

What is corrected calcium?

A

= Total Ca + .8(normal albumin-serum albumin)

[normal generall = 4]

206
Q

How iwll changes in blood pH alter levels of serum calcium?

A

acidosis: albumin is buffer so binding sites decresae
hypercalcemia
alkalosis: more binding sites aviable for Ca to bind so ionized Ca is lowe - hypocalcemia

207
Q

Effects of PTH:

A

Increase Ca blood levels:
increase Ca eabsorption from kidney
Ca resorption from bone
increase hydroxylation of VitD->GI Ca abosorptin

208
Q

Calcitonin efects:

A

gives bone the tone’

Ca deposited in bone

Biochem 1502 (3 decks)

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