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Val cards > Nutrition red blood cells > Flashcards

Nutrition red blood cells Flashcards

1
Q

Why RBCs need to be flexible and how they achieve it

A

The shape, because no nucleus, no mitochondria, there is actin inside the cell that keeps it in this form

Biconcave disk, very skinny

Increase surface area for oxygen exchange

Membrane needs to be very flexible (120 days lifespan) to squeeze in small capillarie

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2
Q

Composition of hemoglobin

A

Tetramer of proteins 2 alpha and 2 beta globin

2 heme groups

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3
Q

What kind of compound is heme and what structure it has

A

It is a special product of AAs

It is called pyrrole ring with 4 nitrogens in the center

and iron is connceted with 4 bonds with N and 2 with oxygen-> coordination muber of 6

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4
Q

What AAs binds Fe in hemoglobin

A

Histidine

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5
Q

Myoglobin is

A

Monomeric polypeptide chain with heme in thce center

Myoglobin will accept oxygen from hemoglobin in capillaries, that will provide oxygen for aerobic metabolism in muscles (generating through continuation of TCA cycle)

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6
Q

Third type of hemoglobin

A

Fetal hemoglobin ( 2 alpha and 2 beta chains)

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7
Q

What is oxy,deoxy,carboxy hemoglobin

A

Oxy-> oxygen bound to iron (bright red)

Deoxy-> no oxygen bound to iron (darker red)

Carboxy (CO bound)- cherish red, binds more strongly then oxygen

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8
Q

What minimum hemoglobin should be bound to oxygen and with what equipment

A

Pulseoxymeter (measures the difference between color of oxy and deoxy-Hb)

SPO2 95% anf higher, if below 90% ->problems breathing

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9
Q

What is carbamino -Hb

A

CO2 bound to globin part of Hb

It contributes to a quarter of CO2 transportation

Co2 is also more strongly bound to Hb than oxygen

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10
Q

NO is ___ and binds to

A

It is a vasodilator that binds to globin

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11
Q

Why something binds to globin, in what state is iron

A

Fe 2+

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12
Q

What is Met-Hb

A

Oxidized iron (brown color in raw hamburgers)

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13
Q

How glucose gets inside RBCs

A

GLUT 1- keeps the concetration is the same as in plasma (5 mmol/L)

and then it is converted quickly to G6P to capture inside glucose

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14
Q

In chronic hyperglycemia what happens to glucose that get inside the RBCs

A

Glucose+Hb-> increase of HbAc, non-enzymatic glycation

Should be 5% ( in normal people)

in diabetic from 6.5-11%

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15
Q

What do we need to do to keep RBCs healthy

A

Keep electrolytes (Na-K Atpase)

Generate ATP by glycolysis, no futher , because no mitochondria. the end is pyruvate, which is converted to lactate and send to cori cycle

NADH that is generated through glycolysis help to reduce iron

To keep the cell protected from free radicals-> glutathione. G6P dehydrogenase that takes glucose through the pathway that will generate NADPH and that will reduce GSSG to GSH

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16
Q

How do we control oxygen release from RBCs

A

We have an isomerasition of 1,3 diphosphoflycerate to 2,3, that binds with hemoglobin more and prevents release of oxygen and results in keeping HbO2 in its oxidized state

So energy state of the cell and the level of ATP that is going to influence the proportion of 1,3 and 2,3

In tissues we have more 1,3 and less 2,3 to release oxygen

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17
Q

How fetus its oxygen supply

A

Through maternal circulatory system, there is a pool of mother’s blood in placenta

Fetal hemoglobin is hungrier for oxygen (because of alittle different AA profile) than maternal hemoglobin, at any oxygen concentrations fetus is going to capture oxygen from mother

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18
Q

What happens with baby when he is born and does not get ocygen from mother

A

New hemoglobin is going to be synthesized to adult hemoglobin

A complete turnover of RBCs in 2 month+ growing-> huge requirement iron

Get in breast milk

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19
Q

How baby can meet the needs for iron from breast milk if milk is low in iron

A

in milk higher availability, because it is in the form of lactoferrin (2+ Fe)

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20
Q

What type of disesase is G6PD deficiency

A

Genetic, X-linked, recessive, many SNPs

people who are homozygous recessive

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21
Q

How G6PD can be bad and good

A

There can be some crisis, that sets up oxidative stress due to lack of glutathione

Can be infection or fava beans (prooxidant)

Higher AGE’s, hemolytic anemia, increased bilirubin, jaundice

But protection against malaria (some drugs agaisnt anemia are toxic to people with G6PD deficiency

Jaundice is a condition that causes skin and the whites of the eyes to turn yellow.

AGE’s-Advanced glycation end products (AGEs) are proteins or lipids that become glycated as a result of exposure to sugars.

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22
Q

Describe iron metabolism

A

We absorb iron as Fe 2+

Free iron is toxic, so it is always should be bound to protein

Ferritin (3+) inside the cells (enterocytes) and then on the basal lateral side we have ferroportin that escortes iron out. Iron is brought to transferrin.

Transferrin trasnports iron to the bone marrow.

In bone marrow iron (2+) is combined with protoporphyrin->heme and then it is added to already existing globular proteins.

Hb take out nucleus->RBCs for 120 days

All RBCs go to the liver to be catabolized. Heme is converted to bilirubin

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23
Q

What happens to iron metabolism when we become iron deficient

A

We use iron stores (ferritin)

  1. Depletion of iron stores
    – decreased plasma ferritin
  2. Changes in iron transport
    – increased absorption efficiency
    – increased transferrin iron binding capacity
    – decreased transferrin saturation %
    – increased transferrin receptors
  3. Defective erythropoiesis
     decreased plasma iron
     Erythrocyte protoporphyrin
  4. Iron Deficiency Anemia
     Microcytic hypochromic erythrocytes
     Associated behavioural signs
24
Q

Iron is bound to protein in what form

A

Fe 3+ and it functions as Fe 2+

25
Q

What acute phase protein is trasnferrin

A

Positive

26
Q

Why when we have an infection or cold transferrin increases?

A

It keeps iron from invading pathogens, because they need iron to replicate, so we sequesture all iron in proteins

27
Q

The other case when we have increased concentration of trasnferrin (not infection)

A

Iron deficiency, because we have 6 binding sites on trasnferrin and to be more efficient in absorbing iron, we make more transferrin, so we can bring more iron to bone marrow

28
Q

Do we have big storage of iron

A

No, it is actually low, most of iron is working iron in RBCs or in other proteins

29
Q

Most of ferritin is stored in

A

Liver

30
Q

Causes of iron deficiency

A
  1. Decreased dietary iron
    – Less iron absorbed
    – Vegetarian diets lack heme
  2. Inhibition of absorption
     Mineral Interactions: Calcium, zinc
    supplements can  iron absorption
     Absorption inhibitors

If iron is in 3+-> not absorbed
3. Increased red cell mass
 Pregnancy, growth
4. Increased losses
 hemolysis
 GI bleeding (occult)
 Heavy menstrual losses

31
Q

How vitamin E can be related to hemolysis

A

It is antioxidant, that is fat-soluble, keeps integrity of cell membranes

32
Q

How heme iron is absorbed and released

A

Heme Iron
• 25% absorbed
• Absorbed as heme
• Fe released in
mucosal cell

33
Q

What to do if diagnosed with iron deficiency

A

Take iron and then retest ( did dietary iron made a difference), if not than looking for problem in absorption or increased losses

34
Q

Absorption of non-heme iron

A

Absorption highly
variable: 1‐50%
absorbed, average <10%
– Released from ligands
by gastric HCl
– Absorbed as Fe2+
reduced ferrous iron not
as Fe3+ oxidized ferric
iron

35
Q

There is one AAs that is very importnat in making Hb, its deficiency can cause low hemoglobin

A

Histidine

36
Q

RDA for iron fo rmen and women

A

Men -8

Women -18

37
Q

Iron deficiency anemia cut offs

A

Hb<140 in men, 120 mg/l in premenopause women, 140 in postmenopausal

38
Q

What is hepcidin

A

Hepcidin is a key regulator of the entry of iron into the circulation in mammals from intestine or stores. synthesized in liver

It is master regulator of iron

Its job is to sequesture iron in these stores, so that pathogens do not have a chance to use it

IL-6 stimulates hepcidin pathway in the liver

39
Q

What is the action of hepcidin

A

It binds to feroportin, internalizes it and targets it to be broken

So if there is less feroportin-> iron does not get out, it is still bound to ferritin, so after three days intestinal cell turnover and we do not absorb iron at all

we are deficient (it is usually decreased-> more ferroportin->more absoprtion)

40
Q

Draw a cheme of iron pathway

A
41
Q

Why it is not good idea to foritfy all products with iron

A

Hemochromatosis: (chronic iron overload with tissue damage)
5+ types - Autosomal recessive
Defective regulation of hepcidin synthesis (decreased)
Increased ferroportin synthesis
Very efficient iron absorption
Iron deposition as hemosiderin, –cirrhosis

Men will at risk more,because they has less losses

42
Q

What is the response of the organism to decreased oxygen supply

A

Secretion of erythropoietin, a hormone that stimulates the bone marrow to produce more RBCs

43
Q

Stages of RBC developmentProery

A

Proerythroblast in bone marrow

Erythroblast

Then early intermediate phase,where DNA decreases, nucleus extruded,mitochondria disappear

Reticulocytes->blood->mature erythrocytes

44
Q
A
45
Q

How erythropoietin secretion is stopped

A

Negative feedback to kidneys, when increased O2 supply

46
Q

How atheletes can play around with erythropoietin

A

They can train in high altitutes, so increased RBCs count

Nee to come to olympics ahead of time

If you can take exogenous erythropoietin, you can have increased endurance

Or to sleepin low oxygen environment

47
Q

What is one unit of heme made of and how it is made

A

Aminolevulinate subunits are connected together

Succinyl CoA(from TCA cycle)+ Glycine-> (with ALA synthease) to aminolevulinate

Then PBG sythase connects Aminoevulinate into porphobinogen

PBG deaminase connects 4 of this units into the chain and they are connected in cyclic form

Decarboxylase finish the formation of heme, so nitrogens are getting ready to accept iron

Ferrochelase puts iron onto heme, finishing the reaction

48
Q

What is acute intermittent porphyria

A

decrease synthesis of PBG deaminase, the problem is that there is an increasse in precursors but decrease in heme.

Usually heme will stop the sysnthesis reaction by negative feedback, so more ALA. It is toxic to neurons and produce psychiatric problems

Treatment of AIP is high CHO diet, it will decrease the production of precursors or get some heme precursors that will result in negative feedback, in very bad cases glucose through IV

49
Q

What is porphyria cutanea tarda

A

decarboxylase is blocked, results inchanges in the skin when it is exposed to sunlight, in may increase hair growth, blistering and darkening in the skin. The therapy is to stay out of the sun

50
Q

Sickle cell anemia is the result of

A

SNP (autosomal recessive)

Glutamic acid is changed to Valine

51
Q

Sickle cell anemia ressembles G6PD deficiency how

A

Homozygous- not good

heterozygous- protection against malaria

Lactose persistent also a survival mechanism

52
Q

Difference between homozygotes and heterozygotes sickle cell anemia

A

• Homozygotes
– Hb polymerizes under
low oxygen tension
– RBCs sickle, get stuck,
ischemia
• Heterozygotes
– Resistant to malaria

53
Q

Heme is degraded where and how

A

In the liver

Protein is broken down thorugh proteolysis

Heme is degraded firstly by breakig the cyclic structure into the chain (biliverdin) and then we convert it to bilirubin

54
Q

Who we exrete bilirubin if it is not soluble

A

Conjugated. In the liver, bilirubin is conjugated with glucuronic acid by the enzyme glucuronyltransferase, making it soluble in water: the conjugated version is the main form of bilirubin present in the “direct” bilirubin fraction. Much of it goes into the bile and thus out into the small intestine.

Some of it is excreted through bile, which is going to be converted to stercobilinogen by bacteria (color of feces).

Or bilirubin diglyconuride (conjugated type) can go to kidneys and be excreted through urobilinogens

55
Q

What is jaundice

A

Another term is (icterus)

Accumulation of biliruin in different tissues

The result of increased need to degrade heme , when increased RBCs degradation, hemolytic anemia, like in malaria, also when there is liver disease

Or Liver can be fine, but there is a problme in removing of bilirubin, the problem in bile duct (cholestasis, bilary atresia)->pale feces, dark urine

56
Q

How neonates can have jaundice

A

Babies can have not such developed liver function or not be able to produce bilirubin or to get read of it

Babies can have lighter feces because they do not have bacteria yet, not mature liver

Can make an exposure to UV light to help break bilirubin

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