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
2
Q
What is kwashiokor?
A
Pathological rapid response with high mortality decreased protein intake (stress) edema ABnormal albumin levels immune function compromised
3
Q
What is Protein energy malnutrition?
A
Low caloric and Low protein intake
accompanied by micronutrient deficiencies
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
5
Q
Why are elderly patients at high risk for malnutition?
A
Depression Meds GI tract aging lower sense of taste B12 deficiency
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
7
Q
What are the ABCDs of nutrition classification?
A
Anthropometric
Biochem lab tests
Clinical Signs
Diet History
8
Q
What are some anthropometric measures?
A
Weight
BMI
Skin fold thickness
Arm circumference
9
Q
What non-nutritional factors can effect albumin levels?
A
Injury/disease
Kidney disease
Liver disease (cirrhosis)
Dehydration status
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
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
12
Q
What markers can you use on a short term basis for nutritional status?
A
serum transferrin free albumin (this is not albumin)
13
Q
Describe acute metablic adaptations to starcation
A
Decrease in muscle mass
ketones
alanine for gluconeogenesis
Glucose to the brain
14
Q
describe chronic metabolic adaptations to starvation
A
break down of stored fat
reduced alanine and glutamine
Ketones to the brain !
15
Q
What is refeeding syndrome characterized by?
A
hypophosphatemia
hypokalemia
hypomagnesemia
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
17
Q
Which nutrients are needed for Hb sunthesis?
A
B12, folate, iron
18
Q
What is the creatine-height index?
A
measure rebuilding of muscle mass
muscle mass/lean body mass
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
20
Q
What problems are associated with obesity?
A
Metabolic syndrome DM CV disease HTN depression stroke apnea
21
Q
What is the formula for BMI?
A
BMI = lbs / (in^2) X 703
22
Q
What is the normal range of BMI?
A
18.5-24.9
23
Q
How good of a marker is BMI a measurement for fat?
A
in children: good
in college kids: toss up, doesnt matter
24
Q
What waist measurements indicate higher risk of disease in men and women?
A
men: <35 in
25
What is calipers?
measurement of subcutaneous fat
26
What is the heritability for BMI in adults and children?
~ 0.7
27
What gene is most strongly supported by evidence to be linked with obesity?
FTO
fat mass and obesity associated gene
involved in demethylation of nucleic acids
28
Where is the higheest concentration of FTO expressed?
hypothalamus
| also adipocytes and nuclei
29
What is the risk allele for FTO associated with?
associated with decreased lipolysis in adipocytes
30
What are the allele forms of FTO?
AA: high risk of increased BMI
AT: middle risk
TT: low risk
31
What diseases can cause serum albumin to be decreased?
liver disease
kidney disease
poor nutrition
inflammation
32
On which FTO allele type does physical activity have the biggest impact>
AA
33
What can adipose tissue release as an endocrine organ?
adipokines
leptin etc.
high adipokines i nobesity
34
Describe leptin and its role in appetitie/energy expenditure
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)
35
What does the stimulation of anorexogenic neurons release?
expression appetite inhibiting factors:
POMC
CART
36
What does the stimulatio nof orexogenic neurons release?
inhibition of of appetit stimulation factors:
Neuropeptide Y
AgRP
37
How is energy expenditure increased with lectin activity?
sympathetic nerve activity in brown adipose tissue to stimulate thermogenesis
38
Compare effects of leptin and insulin
both decrease appetite and increase E expenditure
39
What molecule help regulate appetite?
```
leptin
insulin
ghrelin
cholecystokinin
glucose/lipids
```
40
What is the effect of leptin in skeletal muscles?
promotes insulin sensitivity
41
What is the relationshp bw leptin and AMPK?
Leptin stimulates AMPK -> phosphorylates regulatory enzymes ->
stimulates fatty acid biosynth
42
What is the rate limiting / commited step in fatty acid biosynth?
ACC enzyme
(acetyl coA -> malonyl coA)
ACC switched off when phosphorylated
43
If ACC is phosphoraylted, what happens?
ACC is inactivated
so decreased production of malonyl CoA
This stimulates CPT1
44
What does CPT1 do?
Transports fatty acids from cytosol to inner membrane (mitochondrial matrix) where fatty acids are oxidized
45
How are fatty acid oxidation and fat deposition related?
incerased oxidation leads to less deposition in skeletal muscle
decreases risk of DM2
46
What happens to leptin levels in obese patients?
Increased
| because of leptin resistance, impaired signaling
47
What can exercise induced activation of AMPK lead to?
enhance mitochondrial biogenesis and
| GLUT4 transporters in skeletal muscle
48
How does AMPK influence whole body energy metabolism?
Inhibits ATP anabolism (cholesterol, f.a. synth)
Promotes ATP catabolism (fatty acid oxidation)
also a nutrient sensor in fed and unfed state
49
How can metformin influence AMPK in different tissues?
Stimulates AMPK in liver and muscle
| Inhibits AMPK in hypothalamus
50
What is the effect of metformin on the hypothalamus?
inhibits AMPK so decreases appetite
51
Decreases in leptin are associated with what changes in neuroendocrine function?
Decreased Thyroid hormone
Decreased IGF-1
Decreased Repro hormones
(all for lower E expenditure)
52
What can mutations (rare) in the leptin gene produce?
hyperphagia (excessive hunger)
obesity
leptin injection corrects this
53
What mechanism might enable leptin to assist in weight loss?
Weight loss decreases insulin and leptin resistance
| Now, leptin can perform normal function of reducing appetite
54
What medical disorders are associated with acquired leptin deficiencies?
Eating disorders:
| anorexia, bulemia
55
What are the sensitive periods of adipocyte dev. during growth?
1) 1st year of life - increase in volume (hypertrophy)
| 2) prior to puberty - increase in # (hyperplasia)
56
What are teh six categories of nutrients?
```
carbs
lipis
proteins
vitamins
minerals
water
```
57
What disease exhibits the highest death rate in our population?
heart disease
58
What does the Dietary Reference Intake include?
Estimated Average Req (EAR)
Recommended Dietary Allowance (RDA)
Adequate Intake (AI)
Tolerable Upper Intake Level (UL)
59
What are teh 3 essential energy uses?
basal metabolic needs
food intake effect
physical activities
60
What is the Estimated Average Requirement?
intake at which risk of inadequacy is 50%
61
What factors influence BMR?
lead body mass
growth
fever and disease
cold temps
62
How much does the BMR contribute to daily energy expenditure?
60-70%
63
Daily Value is absed on which dietary standards?
Daily Reference Values
| Referenec Daily Intake
64
Which tissues are normally dependent on carbs?
brain
renal medulla
RBCs
65
What is the acceptable carb intake of carbs?
45-65% of caloric intake
66
Below what gram level of carbs can lead to problems? What kinds of problems?
Below 60g/day carbs
| ketosis, tissue breakdown, cation loss (Na), dehydration
67
What are some water soluble fibers?
pectin
gums
mucilages
some hemicellulose
68
Wat are some water insoluble fibers?
cellulose
lignin
most hemicellulose
69
How do soluble and insooluble fibers benefit you?
soluble: daley emptying, lower cholesterol by binding bile acids (small intestines)
insoluble: accelerate emptying, dilutes fecal mutagens by increasing fecal weight (large intestines)
70
What are the AIs of fiber intake for men and women?
men: 38g/day
women: 25g/day
71
Which of the macronutrients are non-esential?
carbs
72
What are examples of disaccharadies?
lactose
| maltose
73
What are some function of proteins?
builind and reparing tissues
purine, pyrimidine, heme snth
plasma protein synth (albumin)
74
What are essential amino acids? What are they?
required by body
but not produced by body - must be ingested
PVT TIM HALL
75
Where is protein turnover highes? lowest?
Highest? intestinal mucosa, liver, pancreas, kidney, plasma
| Lowest: muscle, brain tissues
76
What is significant about muscle protein and amino acid reserve?
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
77
What is Nitrogen balance?
metabolic balance bw body;s intake and output of Nitrogen (dietary protein)
78
What is the ratio of protein consumption and N2 excretion?
for every 6.25g of protein consumed, 1g N2 excreted
79
What conditions will cause negative Nitrogen balance?
Greater N2 output than input:
inadequate dietary protein
lack of essential a.a.
metabolic stress
80
What conditions can cause positive nitrogen balance?
growth
pregnancy
lactation
recovery from metabolic stress
81
What a.a. deficiencies can be casued by exclusive eating of corn? wheat? beans?
corn: Trp , Lys
wheat: Lys
beans: Met
82
What percent of total energy supplied by protein is adquate?
12%
83
What are the main function of lipids and fats?
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)
84
Which essential fatty acids are omega-6?
linolEIC acid
| arachidonic acid
85
What is the principal funciton fo essential fatty acids?
```
precurosrs of local hormones:
leukotreines
prostoglandins
thromboxanes
(BUT ex: PGs from omega 3 varies from PGs of omega 6)
```
86
What are exampels of dietary poly unsaturated fats? What are their benefits?
omega-6:
vegetable oils (corn, bean, sunflower)
Decrease plasma total and LDL-cholesterol
87
What are some examples of monounsaturated fats?
olive and canola oils
| Decrease plasma and total LDL cholesterol
88
How can fish oils prevent CV diseases?
```
omega 3s:
antiarrhytmia (major)
TAG lowering
HR lowering
BP lowering
Antithrombosis (minor)
```
89
What are some antioxidants that can protect fats from goign rancid?
BHA
BHT
Vit C
Vit E
90
What are the water soluble vitains?
```
B1 - Thiamin
B2 - Riboflavin
B3 - Niacin
B6 - Pyridoxine
B12 - Cobalamins
Pathothenic acid
biotin
folate
Vit C
```
91
Which of the wtaer soluble vitains can be stored inthe body?
B12 - Cobalamins
92
What coenzyme is thiamin metabolized to? Where are its funcitons?
thiamin pyrophosphate
| TCA cycle, glucose metab, nerve impulses
93
What are varying severity of symptoms from thiamin (B1) deficiency?
moderate: in chronic alcoholics (wenicke korsakoff syndrome)
| less severe: elderly
94
What coenzyme is Riboflavin metabolized to? What are its functions?
FAD and FMN
| redox
95
What are symptoms of Riboflavin (B2) deficiencies?
angular cheilitis (mouth fissures)
glossitis
scaly dermatitis
96
What coenzymes is Niacin (B3) metabolized to? Functions?
NAD+ and NADP+
| redox
97
Symptoms of Niacin (B3) deficincy?
pellagra
3Ds: dermatitis, diarrhea, dementia
moderate: lethargy, nervousness
98
What can pharmological doses of Niacin do?
vasodilation
decreased mobilization of fattty acids from fat tissue
decreased cholesterol levels (LDL)
(this can help with hyperlipidemia)
99
Which Vitamin defiecincies are related to alcoholics?
Thiamin
Riboflavin
Niacin
Folic acid
100
What coenzyme is Pyrodoxine (B6) metabolized to? Fnctions?
```
pyridoxal phosphate
catalyze (4):
transaminations
deaminations
decarboxulations
condensations
energy catabolisms, neuro, heme
```
101
Which vitamin is responsible for the conversion of tryptophan to niacin?
pyridoxine (B6)
102
What vitamin should women taking contraceptives take?
double dose of pyridoxine (B6)
103
What coenzyme is pathothenic acid metaabolized to? Function?
CoA and phosphopantotheine
| CoA for acyl transfers
104
Which vitamin is not recognized with any diseases?
pantotheni acid
105
What is the fucntion of biotin? Where is most of it produced
for carboxylation reactions (for glucose, f.a., succinyl CoA)
intestinal flora produces half of daily supply
106
What food intake can lead to biotin deficiency?
raw egg whites
| avidin protein binds biotin so tight that it cant be absorbed
107
What is berberi?
neuromuscular symptoms
atrophy and wekaness of muscles
edema
heart failure
108
What is sideroblastic anemia? When will you see it?
microcytic anemia in presence of adequate Fe
| seen in B6 deficiency
109
What are the hematopoietic vitamins? Why are they called so?
Vitamin B12 and folic acid
| Because these deficiencies first efect hematopoiesis
110
What are the two active forms of Vit B12
adenosyl cobalamin
| methyl cobalamin
111
What is the ingested form of B12?
| OTC form?
ingested: hydroxy-cobalamin
OTC: cyano-cobalamin
112
What is required for the absorption of B12?
Intrinsic factor, IF
| Secreted by parietal cells
113
What type of anemia is observed with B12 deficiency?
megaloblastic anemia (macrocytic)
114
What is pernicious anemia?
inability ot utilize/absorb B12
lack of intrinsic factor from autoimmune rxn that destroys paietal cells
more common in elderly
115
What may vegetarians be prone to?
B12 eficiency since plants have no B12
116
Can plants or animals synthesize B12?
Neither can
| absorption from bacteria that produces it in gut flora
117
In nature, how many glutamic acid residues can folate contain?
7
118
Which form of folate can humans absorb? Describe the process in the body
monoglutamate form of folate
conjugase (in brush border) hydrolyzes the poly form
transported to tissues
Then polyglutamated (ACTIVE coenzyme form)
119
What must happen to polyglutamated folate in order to carry 1-carbon units?
Must be reduced to tetrahydrofolate form
120
What is methotrexate?
a folic acid analogue used to treat:
psoriasis
RA
neoplasms
121
Describe how B12 deficiency interferes with nucleic acid biosynth
"methyl folate trap" - methione synthase enzyme may be bad
Homocystein-> methion rxn is blocked
accumulation of methyl-FH4 and lack of FH4
122
Which vitamin is the easist to become dificient?
| What is the requirment?
Folic acid
| 400 microgams/day
123
What can a lack of folate during pregnancy lead to?
Neural Tube Defects
124
What is the coenzyme form of Vit C? Functions?
```
ingested form
hydroxylation of prolyl and lysyl in collagen
iron absorption
antioxidant
prevents cataracts
```
125
What may lower Vit C serum levels?
smoking
oral contraceptives
corticosteroids
Stress
126
Which types of vitamin deficiencies are seen in microcytic, normocytic, and macrtocytic anemias?
micro: Fe, B6, Vit C
normo: protein/energy malnutrition
macro: B12, folate
127
Which vitmain is invoved in heme biosynthese?
B6
128
Which fat soluble vitamins are endogenously synthesized?
D (skin)
| K (intestinal flora)
129
Which fat soluble vitamins are converted to active forms in the body?
Vit A and D
130
What is the most abudant caretonoid eaten by people?
B-carotene
131
What family is Vitamin A a part of? Where do they come from?
VitA part of retinoids
Come from provitamins A (caretinoids)
1 caretnoid is cleaved into 2 VitA
132
How much is 1 retinoid equivale equal to?
1 RE = 6 microg B-carotene and 12 microg of other caretinoids
133
What form is dietary vitamin A mostly in?
retinyl esters in the fatty portions and
| B-carotene from plants
134
Whiat areas does Vitamin A functino in?
vision
gene regulation
antioxidant
135
How do dietary retinyl esters eveentually end up in the liver or adipose tissue?
retinyl esters are hydrolyzed to retinol.
Retniol is transported into mucosal cells
Re-esterified and go into chylomicrons to liver
136
How much supply can the liver store vitamin A?
6-12 months
137
What proteins make up rhodopsin? What is its role in vision
opsin and 11-cis retinal
| light induced conform. change of opsin produces nerve impulse mediated by cGMP
138
Which form of vitamin A fnctions in gene regulation?
all-trans retinoic acid in epithelial cells
139
What can occur from Vitamin A deficiencies?
keratin build up:
| xerophtalmia - corneal keratinization
140
How is active form of Vitamin D formed from sunlight?
7-dehydrocholesterol (skin) converted to cholecalciferol -> 25-OH-cholecalciferorl (liver) -> 1,25-diOH-cholecalciferol (kidney)
141
What form is dietary vitamin D given in?
Vitamin D2 - ergocalciferol
142
What is the funciton of the active form of Vitamin D (1,25-diOH-calciferol) ?
induces synthesis of protein for Ca absorption in intestinal cells
Acts with PTH to increase blood Ca levels (homeostasis)
143
What can Vitamin D deficiencies cause in varying age populations?
children: rickets
adults: osteomalacia
144
How many chemical form sare there for Vitamin E ?
8
145
Which of the vitamin E chemical forms meets human requirements ?
alpha-tocopherol Vitmain E
146
What is the main function of vitamin E?
antioxidant
147
What is seen in hypovitmainosis in Vitamin E?
fragility of RBC membranes
148
What is the main funcitno of Vitamin K?
cofactor in gamma carboxylation of glutamates in:
precoag. factors - 2, 7, 9, 10, C, S
bone proteins
149
What are some preisponsing conditinos of Vit K deficiency (hemhorrage) ?
parenteral nutrition
malabsorption syndrome
liver dysfunction
150
How much of alcohol is oxidized in liver?
80-90%
151
What is the common product of the main pathways of alcohol metabolism?
acetaldehyde (very toxic)
152
What are the 2 main pathwasy for alcohol metabolism?
```
alcohol dehydrogenase (ADH) of cytosol (stomach, liver)
microsomal etahnol xoidizing system in ER (liver)
```
153
How is first pass metabolism/gastric barrier lost in alcoholism?
decrease in gastric ADH activity from gastritis
154
2 reasons why female alcohol blood levels are higher than males
higher fat content proportion
| less gastric ADH activity, so more enters blood
155
What is the most important metabolic effect of alcohol? What are other conditions?
```
generation of NASH in liver- overwhelms liver
lactic acidosis
scondary hyperuricemia
TCA cycle depressed (NAD slowing)
hypoglycemia
fatty liver
```
156
Where is the site for the adaptive system of ethanol oxisdaation (MEOS) ?
liver microsomes
157
What types of enzymes oxidize alcohol?
cytochromeP450
| -2E1
158
Which enzyme is induced during chronic alcohol use?
2E1
This induction leads to metabolic tolerance EtOH
(Hepatic ADH is not inducible)
159
Under what condition is P4502E1 most effective?
When large aounts of alcohol are consumed
160
In which individulas is P4502E1 most effective?
alcoholics
161
The enhanced metabolism of which drugs are seen in alcoholics?
analgesics (acetomenaphin, pentobarbital, cocaine)
162
In the presence of high 2E1, tylenol is broken down to which toxic metaboliter?
NAPQ1
163
Increase in P4502E1 may partially account for...
increased incidence of cancer in alcoholics
testicular atrophy
gynecomastia
164
The effect of which enzyme is diminished with chronic alcoholism?
Aldehyde Dehydrogenase (ALDL)
diminshed activity leads to build up of acetylaldehyde
highly reactive via oxidative damage
165
What is Ernicke-Korsakoff Syndomre?
severe thiamin deficiency
ataxia
ophthalmoplegia
mental confusion
166
What is the cause of cirrhosis
toxic effect of alcohol and
| malnutrition
167
What is a potential treatment ofr alcoholism?
Disulfiram
| conidtioned avoidance response to acetaldehyde build up
168
When is stomach oxidation of alcohol decreased?
in alcoholics
in women
gastritis
drugs with alcohol
169
Which minerals are essential micronutirents?
```
Iron
Ca
Mg
An
Cu
Se
```
170
Why is iron essential for life?
transport of compounds and oxygen
| hemoglobin
171
What are some heme proteins?
hemoglobin
myoglobin
various cytochromes
172
What are some non0heme iron proteins?
Fe-S cluster proteins
173
Where are teh 2 major storage sties of iron?
reticuloendothelial macrophages
| liver
174
What is transferrin?
transports iron between utilization and storgae sites
175
how much iron does the body contain?
2-4 g
176
Which iron form is quantitatvely more present? which is more biologically active?
quantitatively: non-heme
active: heme
177
What are 3 observations of unique iron requirements?
Pregnancy requires more iron (27)
Postemenopausal requires less (8mg)
1st 6 months of life is very low requirement
178
What is ferritin?
protein that sequesters iron and binds extra Fe
179
What is the path of heme-Fe uptake in a cell?
heme -> HPC1-> HO -> then either stored or used
180
What is ferroportin/IREG1?
transport protein that moves Fe out of cell
| hepaestin (Cu) also needed for this
181
What form is iron from a diet?
Fe 3+
182
How can Fe 3+ be reduced to Fe2+ ?
- Ferric Reductase (DytB) - brush border
| - Vitamin C
183
What are enhancers of absorption of iron?
VitC
citrate
meat factor
reducing sugars
184
What are inhibitors of iron absorption?
phytates, calcium, tannates, carbs...
185
What is iron homeostatsis regulated by?
hepcidin
- synthesiezed in liver
- prevents iron transport across gut and inhibits iron absorption when Fe levels are high
- also traps iron inside macrophages
186
How does hepcidin work?
```
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
What 3 proteins are involed in hepcidin regulation?
HFE, TFR2, HJV
188
How will the hepcidin-ferroportin system be altered in iron defiecient patietns?
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
How will the hepcidin-ferroportin system be altered in infectous patients?
Since antimicrobial, hepcidin will be upregulated
also less Fe mobilization and less absorption
starves bad bacterioa of iron
190
How will the hepcidin-ferroportin system be alteterd in a deleterious mutation of HFE gene?
Regulation is decreased
so decreaed expression of Hepcidin
storage will increase; absorption will increase
191
Describe the 3 stages of iron deficiency?
1: Fe storage being depleted
2: impairment of erythropoeiss
3: overt iron deficient anemia
192
What is the gold standard to test for iron storage?
stainable marrow iron
193
What do serum ferritin levels indicate?
directly proportional to amount of iron stored
| (But also increases with acute phase/inflammation
194
What are the most commonly used test to test iron in erythroid tissues?
```
serum iron
transferrin saturation (TSAT)
```
195
Which test are most sensitive in changes to iron status?
```
stainable marrow iron
serum iron (more practical)
```
196
Which tests are elast sensitive to changes in iron status?
Hb, MCV, MCHC
197
How do soluble transferrin receptor levels change with iron deficiency?
During deficiency, sTFr levels will increase
gene expression goes up
ferritin expression goes down
198
Which subgroup is at higher risk for iron deficiency aemia?
pregnant women
199
Describe anemia of chronic disease
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
Describe herediatry hemochromatosis
autosomal recessive
excess iron deposited in various tissues
most common type: HFE mutation
201
What is the most abundant mineral in the body?
calcium
| 1000g
202
What are normal serum calcium levels?
9-10 mg/dL
| much of which is bound to albumin
203
How will hypoalbuminia effect serum Ca levels?
total calcium levels iwll decrease proportionately
| ionized Ca will remain same though
204
What serum level determines hypo or hypercalcemia?
amoutn of ionized Ca
| difficult to test though
205
What is corrected calcium?
= Total Ca + .8(normal albumin-serum albumin)
| [normal generall = 4]
206
How iwll changes in blood pH alter levels of serum calcium?
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
Effects of PTH:
Increase Ca blood levels:
increase Ca eabsorption from kidney
Ca resorption from bone
increase hydroxylation of VitD->GI Ca abosorptin
208
Calcitonin efects:
gives bone the tone'
| Ca deposited in bone
