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Metabolism-Alaa > blood & Iron > Flashcards

blood & Iron Flashcards

1
Q

why does the spleen carry a reservoir of blood?

A

in case the body goes into some hemmoragic shock, it also has a reservoir of platelets

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2
Q

how do u treat iron deficiency?

A

-dietry advice -oral iron supplements (take with orange juice) - IM iron injection - IV injection -Transfusion ( only is severe anomie)

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3
Q

what is Hepcidin? what secretes it?

A

a negative regulator of iron absorption, targets enterocytes & macrophages by degrading FERROPORTIN. so iron get into the enterocytes but dow not leave it (ma7ad yisafir, fajarna il ma6ar)

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4
Q

______iron is more readily absorbed than inorganic iron (fe2+ and Fe3+)

A

heme

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5
Q

how is iron taken into cells?

A

by binding to Iron transferrin complex onto Transferrin receptor (TFR)

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6
Q

which cell have the highest number of transferrin receptors?

A

Epitheloid cells

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7
Q

where does most of our iron come from?

A

a small amount comes from the diet, but most comes by RECYCLING of old RBC taken up by macrophages in the reticuloendothelial system and returned to the store pool within the body

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8
Q

describe platlets

A

have no nuclei -r actually membrane bound fragments of cytoplasm that budd off from megakaryocytes whose formation is driven by TPO (thrombopoeitin)

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9
Q

function of RBC?

A

-deliver o2 to tissues -carry Hb -generate energy ATP -maintain osmotic equilibrium

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10
Q

what does the HFE protein do?

A

binds to transferrin, inhibiting it affinity for iron

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11
Q

What can disrupt the structure of RBC?

A

.

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12
Q

Explain the significance of the reticulocyte count

A

,

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13
Q

what r the 2 forms of iron that can exist in the body?

A

It can be in an “Available vs Stored form” AVAILABLE: Hb Myoglobin Tissue iron transported iron STORED: Ferritin>95% in hepatocyte haemosideran>5% in kupffer cell

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14
Q

Mutations in the gene coding for which of the following proteins could potentially cause ‘hereditary spherocytosis?’

A

Ankyrin

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15
Q

Which metaboic pathway is the primary source of ATP production in erythrocytes?

A

Glycolysis

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16
Q

how can iron be stored in body?

A

via ferritin or Hemosiderin

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17
Q

how many grams of iron do u need to obtain from the diet?

A

10-15 mg/day

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18
Q

what do u call iron overload?

A

heamochromtoasis

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19
Q

what r different types of macrophages in the body and where r they located? what r their functions?

A

-kuppffer cells>> liver -tissue histiocyte>> connective tissue -microglia>> CNS -peritoneal macrohphage>> perontineal cavity -red pulp macrophage>>spleen -langerhans cell>> skin and mucosa **they remove dead or damaged cells and destroy foreign antigens in the body.

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20
Q

what is the reticuloendothelial system? what is its role? which cells r involved?

A

a network of cells located around the body and is a part of the immune system. it removes dead or damaged cells and indetifies and destroys foreign antigens in blood and tissues. -phagocytic and include monocytes in the blood and different macrophages in tissues.

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21
Q

How does hemolytic anmeia occur?

A

Incread RBC destruction

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22
Q

function of Hb?

A

carries o2 from lungs to tissues carries co2 from tissues to lungs

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23
Q

Explain the term anaemia and understand the underlying mechanisms resulting in anaemia.

A

,

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24
Q

how is iron absorbed in the intestines? and where does this occur? what regulates this process?

A

duedenom and upper jejenum. Hepcidin>> a small peptide that binds to ferroportin causing it to degrade. preventing iron from leaving the cell. (HEP class took up my time and i didnt go to the airport “ferroportin” so i never left )

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25
Q

what is normal Hb levels?

A

male= 130-180 g/L female= 115-165 g/L

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26
Q

describe the structure and cell membrane RBC

A

-anucleate -biconcave discs, flattened depressed centres -flexible disc 8μm diameter >>it shape Facilitates passage though the microcirculation which has a minimum diameter of 3.5 μm.

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27
Q

when do u switch from metal to adult hb?

A

3-6 months of age

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28
Q

describe how Hb is degraded, where does this occur?

A

SPLEEN HB, is degraded into heme and globin,, Globin is broken down into aa Heme is is metabolised into BILIRUBIN, which is taken to the liver via Albumin and is conjugated there and secreted in bile. bacteria in colon deconjugate it and metabolise bilirubin into Urobilinogen >>urobilin and stercobilin. a small amount of urobilinogen is reabsorbed and processed by kidneys which give the yellowish colour of urine.

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29
Q

what is a good diagnosis to measure for the amount of eyrthropoesis happening in the bone marrow?

A

RETICULOCYTE count form blood sample.

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30
Q

how do rbc’s make ATP?

A

1) glycolysis glucose>lactate 2)pentose phosphate pathway G6P metabolised, making NADPH

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31
Q

Describe the sickle cell dosease

A

A point mutation Substitustion of VALINE(hydrophobic) instead of GLUTAMIC ACID(hydrophilic in poistion 6 in the B chain

“Sticky” hydrophobic pocket formed by Val allows deoxygenated HbS to polymerize

Theyre not happy with being on surface and dont want to bind to o2, so theyll bind to another hemoglobin tetramer to hide away

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32
Q

how should iron supplements be taken?

A

with ACID. Vit C ENHANCES absorption of Iron

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33
Q

what can cause jaundice?

A

excess of RBC destruction>>excess bilirubin

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34
Q

what is thrombopoesis?

A

formation of platelets (thrombocytes)

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35
Q

what is a good diagnosis to measure for the amount of eyrthropoesis happening in the bone marrow?

A

reticulocyte count form blood sample.

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36
Q

what senses dietary iron levels?

A

villi of enterocytes

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37
Q

How is thalassemia classified?

A

.

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38
Q

What is thalassameia?

A

Heterogenous group of disorders that r cause by REDUCED RATE of synthesis of normal a or B globin chains. The excess of the globin chain is gunna cause INSOLUBLE AGGREGATES that will ….

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39
Q

what is hereditary hemoachromatis? how can patients present? how can we treat it

A

autosomal ressesive, excessive absorption of iron. CHROMOSOME 6 coding for the HFE protein, which normally binds to transferrin reducing its affinity for iron to it. theres a MUTATION in the HFE gene. since there is no system for excreting iron, it’ll accumulate in tissues causing organ disruption. Ex: liver, adrenal glands, heart, joints, pancreas. ***cirrhosis, adrenal insufficiency, heart failure, arthritis, diabetes. treat w/ venesection Phlebotomy to remove excess iron

40
Q

what is a primary source of iron in infants?

A

via Lactoferrin, an iron-binding protein that is found in human milk.

41
Q

Explain the concepts of a normal range and be able to assess whether a laboratory test is likely to be normal or abnormal.

A

P

42
Q

in what form is iron absorbed?

A

ferrous form Fe2+

43
Q

What do the granulocytes (epwbc) arise from?

A

MYELOBLAST ich arise from common myeloid proginetirer cells

44
Q

why is excess iron dangerous?

A

bc free iron is dangerous, it can produce highly reactive Hydroxyl radicals>> causing damage

45
Q

Inappropriate activsation of ______is associated with ASTHMA & ALLERGY

A

eosinophils

46
Q

how can we get rid of iron?

A

there is NO mechanism for excreting iron, we lose a bit from sweat, bleeding but we cannot actively secrete it from body.

47
Q

what is responsible for maintaining the RBC BICONCAVE shape?

A

The cell membrane: lipid bilayer that has proteins such as SPECTRIN, ANKYRIN, BAND 3 & protein 4.2 they facilitate interactions with the cytoskeletan of the cell which is essential in maintaining its biconcave shape.

48
Q

Hb catabolism?

A

notes?

49
Q

why is free iron toxic to the cells?

A

bc its a transition metal, it acts as a catalyst in the formation of free radicals to form ROS

50
Q

What is erythropoiesis?

A

Process by which rbc r produced in the bone marrow.

51
Q

What is the most common cause of severe sickling syndrome?

A

HbSS=homozygous sickle cell anemia

52
Q

explain why iron from MEAT is more better than iron in GRAINS?

A

iron in meat is directly in the FERROUS form (which is the absorbed form of iron) while in grains its in the Ferric form so we have to cover it first to ferrous so it can be absorbed

53
Q

what is EPO?

A

a 165 amino acid glycoprotein hormone that inhibits APOPTOSIS of CFU-E (colony forming units of the erythroid cell line) proginator cells

54
Q

describe hoe Erythropoiesis is controlled?

A

reduced o2 is sensed by KIDNEYS (interstitial peritubular cell) EPO produced it stimulates release of RBC from marrow rbc rise and Hb rises O2 rises EPO falls

55
Q

Function of spleen

A

O

56
Q

Which of the following is the best dietary source of vitamin B12?

A

Vitamin B12 can only be obtained in sufficient amount from foods of animal origin. Shellfish such as oysters and mussels are a particularly good source as are liver and fish.

57
Q

where does RBC first start forming? (start with early embryo)

A

vasculature of yolk sac, then to embryonic liver after birth>> bone marrow

58
Q

Iron deficiency: describe changes in Blood parameters and Blood Film features…

A

notes.

59
Q

how do u test for iron deficiency?

A

check for serum FERRITIN! reduced levels= ion deficient normal or increased= doesn’t mean they may not have iron deficiency (lana its a CRP it could be raised due to inflammation) Or CHR=reticulcoyte Hb content, BETTER TEST ohhh cooool

60
Q

**if metabolism is altered, RBC’s breaks down much more quickly

A

ok

61
Q

Explain the basics of haemopoiesis and the role of the red blood cell.

A

.

62
Q

How is vB12 associated with neurological disease?

A

Focal demyelination occurs that will affect the spinal cord, peripheral nerves and optic nerves. Depression and dementia can develop too

63
Q

what is hereditary Spherocytosis?

A

gene mutations in the membrane proteins of the RBC’s lipid bilayer. so RBC LOSE THEIR BICONCAVE SHAPE .

64
Q

what foods inhibits absorbtion of iron?

A

tea, coffee, chapati

65
Q

what stimulates the release of EPO from the kidneys?

A

its released in response to a decrease in O2 levels in the blood (hypoxia) therefore stimulating more RBC production.

66
Q

in iron deficiency anaemia, u can get webbing of the oesophagus, that can cause difficulty swallowing, what is the term for this?

A

Plummer–Vinson syndrome

67
Q

**amount of iron in ur body varies as u grow up

A

kids need more

68
Q

how can iron be stored in body? where in the body r they stored?

A

-ferritin and its insoluble derivative hemosiderin -liver, spleen, bone marrow (ferriTIN> tin stores stuff)

69
Q

what is ferrittin?

A

a protein-iron complex that can be taken in by phagolysosomes to form HEMOSIDERIN GRANULES

70
Q

what foods r a good source of IRON?

A

heme and non heme sources

preferebly meat

for vegans…

ready to eat cereal,

soy beans

lentils

71
Q

what is haempooiesis?

A

the production of blood cells and platelets, which occurs in the bone marrow.

72
Q

where r the main sites of haeomoposis in adults??

A

bone marrow of pelvis, skull, sternum,ribs, vertebrae

73
Q

What r some problems that are caused by problem with Hb synthesis

A
  • thalassemia
  • sickle cell disease
74
Q

What are consequences that lead to sickle cell anmeia?

A

.

75
Q

**IRON DEFICIENCY is a SYMPTOM, not a disease

A

so u must find the underlying cause

76
Q

Effects of CO poisoining in Hb?

A

Carbon monoxide (CO) is a poison because it combines with ferromyoglobin and ferrohaemoglobin and blocks oxygen transport. BINDS MUCH MUCH MORE TIGHTLY WITH O2, and is stuck there forever! Unless u increase the amountof o2 in the atmosphere

77
Q

functions of hepcidin

A

Inhibits iron

  • absorption from gut
  • release from stores eg macrophage
78
Q

functions of EPO?

A

glycoprotein hormone, that inhibits the apoptosis of CFU-E progenitor cells, activation of EPO receptors on these cells allow them to develop, proliferate, and differentiate.

79
Q

what are immature RBC called? how long do they to mature into RBC’s?

A

reticulocytes, 1-2 days

80
Q

why do mature RBC more susebtible to oxidative damage?

A

bc they have no nucleus! incase their proteins got destroyed, make shay to make more of em,

81
Q

disease used to describe RBC that has lost its Biconcave shape

A

hereditary spherocytosis

82
Q

Some things affect hb adfinity to o2, describe what causes a rightwards shift and leftwards shift!

A
83
Q

Hb can be in the T state and R state, explain which is which?

A

Relaxed> bound to oxygen

Tensed> not bound to o2

84
Q

what is the effect of BPG?

A

BPG binds to Hb & decreases the affinity for O2.

85
Q

why do trainers train at higher altitudes?

A

If u go to higher altitudes, theres less oxygen,
Those who r in higher altitudes, make more bpg, and the affinity of o2 to Hb is lower, thats why runners train at higher altitudes, to make more bpg, to allow more transport of o2

86
Q

what is the BOHR effect

A

which H and cO2 there is a shift to the right, therefore

􏰅 Binding of H+ and CO2 lowers the affinity of

haemoglobin for oxygen.

low PH

87
Q
A
88
Q

describe the structure of HEME

A
89
Q

what is Anisopoikilocytosis?

A

change in size and shape

90
Q
A
91
Q

explain the process of hematopoiesis, starting from the hematopoeitic stem cell

A
92
Q

The serum iron level is a reliable indicator of iron deficiency and iron overload.

T Or f

A

FALSE Serum iron levels are subject to diurnal variation and so are not a reliable indicator of iron deficiency, they are also reduced in ACD. % Transferrin saturation is used in screening for haemochromatosis

93
Q

lack of Vit B6 u get_______anemia

A

sideroblastic

eat pistachios

94
Q

Patients who are haemolysing need regular folate replacement . why?

A

They require folate replacement as the body’s folate stores only last a few months

95
Q

where do we see bite cells?

A

G6PDH deficiency

stress makes me bite into some heinz ketchup

96
Q
A

Metabolism-Alaa (23 decks)

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