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CVS II > Red Blood Cells Production + Survival > Flashcards

Red Blood Cells Production + Survival Flashcards

1
Q

Define erythropoiesis

A

🔴production

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2
Q

How many 🔴 per day?

A

10¹²

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3
Q

Features of a proerythroblast?

A

1st recognizable cell in erythroid series

large cell w loose, lacy chromatin, visible nucleus + nucleolus, basophilic cytoplasm

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4
Q

What’s the basophilia caused by?

A

large number of polyribosomes involved in synthesis of Hb

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5
Q

Features of basophilic erythroblast?

A

strongly basophilic cytoplasm (blue) made of polyribosomes, condensed nucleus, no visible nucleolus

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6
Q

Features of polychromatic erythroblast?

A

polyribosomes decrease, cytoplasm filled w Hb (pink red)

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7
Q

Features of orthochromatic erythroblast?

A

nucleus condenses, no basophilia (pink) –>uniformly acidophilic cytoplasm

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8
Q

Features of normoblast?

A

cell has cytoplasmic protrusions, expels nucleus (encased in thin cytoplasm) –>engulfed by macrophages

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9
Q

Features of reticulocyte?

A

small number of polyribosomes, when dyed w brilliant cresyl blue, aggregate forming stained network, synthesises 35% Hb

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10
Q

What is Hb synthesised by + %?

A

65% erythroblast

35% reticulocyte

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11
Q

Features of mature erythrocyte?

A

no polyribosomes

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12
Q

How’s 🔴 synthesised from stem cell in red bone marrow?

A
  • hemocytoblast
  • proerythroblast
  • basophilic (early)erythroblast
  • polychromatic (late)erythroblast
  • orthochromatic erythroblast
  • normoblast
  • reticulocyte
  • mature erythrocyte
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13
Q

What stimulates erythropoiesis + causes?

A

low tissue oxygenation eg hypoxia, decrease in Hb, decrease in O2

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14
Q

Describe the process of hypoxia

A
  • stimulus
  • low O2 levels in blood
  • kidney + liver releases erythropoietin
  • stimulates red bone marrow
  • enhanced erythropoietin increases 🔴 count
  • increase O2 carrying ability in blood
  • normal blood O2 levels
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15
Q

Where’s 90% of erythropoietin produced?

A

properitubular cells of kidneys

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16
Q

What’s erythropoietin?

A

heavily glycosylated polypeptide hormone, of 165 AA molecular weight daltons 30,400

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17
Q

What’s iron controlled by?

A

total body iron status
intracellular iron levels
Erythropoiesis
DMT-1 at brush border of enterocyte transporting iron into cells + ferroportin at basal membrane transporting iron from enterocytes into circulation

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18
Q

How + where’s iron absorbed?

A

5-10% absorbed (1mg)in duodenum+jejunum

HCl + ascorbic acid

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19
Q

How’s iron absorption regulated?

A

DMT-1 at brush border of enterocyte transporting iron into cells + ferroportin at basal membrane transporting iron from enterocytes into circulation

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20
Q

Why’s iron needed for 🔴 production?

A

For synthesis of Hb

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21
Q

How much iron in normal western diet?

A

15mg daily

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22
Q

Describe process of Hb synthesis

A
  • 2 irons bind to transferrin
  • transferrin binds to transferrin receptor on cell
  • endocytosis:
  • ferritin or iron in mitochondria
  • transferrin reused
  • ferritin accumulate excess iron
  • lysosomes engulf ferritin + degrade into insoluble storage=hemosiderin
  • iron in mitochondria + simultaneously glycine + succinyl coA condenses under action of rate limiting δ-aminolevulinic synthase in presence of pyridoxal phosphate (vit B6) coenzyme
  • forms δ-ALA
  • in cytoplasm biochemical reactions:
  • 2 δ-ALA condense forming pyrrole =porphobilinogen (PBG)
  • forms protoporphyrin
  • in mitochondria combines w Fe2+ -> haem
  • cytoplasm globin synthesis
  • globin binds w haem -> Hb
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23
Q

What are the diff causes of Iron deficiency?

A
  • reduced intake: red meat + veg
  • malabsorption: coeliac, gastrectomy, gastric bypass, atrophic gastritis
  • chronic blood loss: GI bleed (ulcer, NSAID, carcinoma, colitis), menorrhagia, PNH (paroxysmal nocturnal haemoglobinuria)
  • increased demand: preg, growth spurt
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24
Q

Why does iron demand increased in preg?

A

for increase maternal red cell mass of about 35%, transfer of 300mg of iron to foetus

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25
Q

What’s the treatment of iron deficiency?

A

ferrous sulphate supplement 200 mg 3x daily

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26
Q

What are the metabolic functions of B12?

A

acts as coenzyme for:
-methionine synthase in methylation of homocysteine to methionine in cytosol
-conversion of L-methylmalonyl coA to succinyl coA in mitochondria
(for 🔴 maturation + DNA synthesis)

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27
Q

What does B12 deficiency cause?

A

abnormal + diminished DNA —> no nuclear maturation

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28
Q

What conditions arise from B12 deficiency?

A

Megaloblastict anaemia : active folate forms unformed so DNA synthesis fails
Neuropsychiatric manifestations:peripheral + autonomic neuropathy, subacute combined
degeneration of the spinal cord, optic atrophy, mood-behaviour changes, psychosis, cognitive prob

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29
Q

What are the diff causes of B12 deficiency?

A
  • inadequate intake : vegans
  • malabsorption : FBCM, pernicious anaemia, gastrectomy, ileal resection, coeliac, chronic pancreatitis, crohn’s
  • inherited : hereditary intrinsic factor def, TC def
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30
Q

What’s Food-bound cobalamin malabsorption (FBCM) + causes?

A

in older people impaired ability to release B12 from food
Instrinsic factor intact + clinical manifestations rare
Caused by gastric dysfunction, reduced gastric
acid secretion by:
gastric resection
treatment w proton pump inhibitors
persistent infection w Helicobacter pylori

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31
Q

What’s Pernicious anaemia ?

A

Commonest

autoimmune gastric atrophy so loss of intrinsic factor production

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32
Q

What’s instrinsic factor?

A

made by gastric parietal cells to absorb B12

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33
Q

What’s Crohn’s disease + symptoms?

A

inflammatory boweldisease(IBD) affecting any part of GI

abdominal pain, diarrhoea (bloody if severe inflammation), fever, weight loss

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34
Q

How do you investigate B12 def + what would you see?

A

-Haematological test:
FBC - macrocytic anaemia, leucopenia, thrombocytopenia
Blood film - hypersegmented neutrophils, oval macrocytes
Bone marrow examination- megaloblasts
-Serum B12- plasma homocysteine

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35
Q

What would you see in the investigation results of macrocytic anaemia?

A 
Mean Corpuscular Volume >95 fl
Oval macrocytes on blood film
reduced 🔴+platelets
Megaloblastic change in bone marrow
Hypersegmented neutrophils 
B12 only - Demyelination in CNS
36
Q

Role of folate?

A

for 🔴 maturation + DNA synthesis:

  • as coenzyme for thymidine triphosphate synthesis
  • as coenzyme for remethylation of homocysteine to methionine
37
Q

Why can folate def occur quickly?

A

Daily adult requirement is 100-150µg

, body stores 10-12mg for 4 months

38
Q

What’s dietary folate + response to heat?

A

In liver, leafy veg, yeast

Folate is heat-label so destroyed at high heat

39
Q

What are the diff causes of folate deficiency?

A
  • inadequate intake : 🙁nutrition
  • malabsorption : coeliac, Crohn’s, tropical spruce, 🍺
  • demand/losses : preg, haemolytic, cancer
  • antifolate drugs : anticonvulsants, methotrexate, metformin, (Anti Epileptic Drug treatment reduces folate + B12 serum levels)
40
Q

How does Sulphonamide work as a antimicrobial agent?

A

inhibit folate synthesis + vital for bacteria survival in the case of antibiotics

41
Q

What’s Tropical sprue(TS) + symptoms?

A

acquired malabsorptive condition of probable infectious aetiology
altered small bowel mucosa, chronic diarrhoea, multiple vitamin + nutrient def

42
Q

How do you investigate folate def?

A

-Haematological test:
FBC - macrocytic anaemia, leucopenia, thrombocytopenia
Blood film - hypersegmented neutrophils, oval macrocytes
Bone marrow examination- megaloblasts
-Serum folate; plasma homocysteine elevated

43
Q

What’s the treatment for folate def?

A

Folic acid tablets 5mg daily for 3-4months

44
Q

Where’s B12 absorbed?

A

Ileum

45
Q

Where’s folate absorbed?

A

Duodenum + jujunum

46
Q

How’s B12 transported in plasma?

A

Bound to TCI

TCII for uptake

47
Q

How’s folate transported in plasma?

A

Weakly bound to albumin

48
Q

What’s the usual therapeutic form of B12?

A

Hydroxocobalamin 1mg, im

49
Q

What’s the usual therapeutic form of folate?

A

Folic acid tablets 5mg/d, 3-4mths

50
Q

What’s Hydroxocobalamin?

A

injectable B12 given when prob w absorption from gut

51
Q

What’s TCI?

A

secreted by salivary glands, protects B12 from degradation

52
Q

What are bone marrow failure syndromes?

A

Group of disorders, inherited or acquired that:
affect HSC which involves cell lines
replace marrow w malignant cells
–> failure of erythropoiesis

53
Q

What can affect HSC by involving cell lines?

A

Aplastic anaemia

54
Q

What are the diff types of Aplastic anaemia?

A

Congenital: Fanconi anaemia, Dyskeratosis congenital
Acquired: Drugs, Radiation, Malignancy

55
Q

What causes the bone marrow to become malignant cells?

A

Leukaemia, lymphoma

56
Q

What are the diff stresses put on 🔴?

A

lifespan 120 days
300 miles travelled via microcirculation
8μm diameter
capillaries 3.5µm

57
Q

What does 🔴longevity depend on?

A

deformability
E supply for cation pump
NADPH supply against oxi-stress
cytoplasmic E involved in metabolic pathways

58
Q

Define 🔴 deformabilty

A

squeezing via splenic sinus

59
Q

Diff ways haemolytic anaemia can be aquired?

A
  • Immune: autoimmune, alloimmune, drug induced

- Non immune:🔴fragmentation, infection, secondary

60
Q

Diff ways haemolytic anaemia can be hereditary?

A
  • 🔴 membrane disorder: spherocytosis, elliptocytosis
  • Haemoglobinopathies: sickle cell diseases, thalassaemias
  • 🔴 enzymopathies: G6PD def, PK def
61
Q

Features of hereditary spherocytosis?

A 
Loss of membrane integrity --> spherical 🔴
Common in N. Europe.
def in proteins w vertical interactions between membrane skeleton+lipid bilayer - spectrin, ankyrin
62
Q

Features of hereditary elliptocytosis?

A

mutations in horizontal interactions eg spectrin-ankyrin, protein 4.1

63
Q

What do mutations or deletions of globin chains lead to?

A

Abnormal synthesis - Sickle Cell Diseases.

Reduced rate of synthesis - Thalassaemia

64
Q

What are the genes on chromosomes 16 + 11?

A

16 - zeta ζ, α1, α2

11 – epsilon, γglutamic, γalanine, δ, β

65
Q

What are the 3 types of Hb in normal adult blood?

A

HbA (α2β2), HbF (α2γ2), HbA2 (α2δ2).

66
Q

What’s Sickle Cell Disease + diff types?

A

Group of Hb disorders w/inherited sickle β-globin gene
-Homozygous Sickle Cell Anaemia (Hb SS) COMMON
GAG -> GTG so Val
-heterozygote conditions (HbS/ βthal, HbSC, HbSD)
HbS/βthal, MCV & MCH lower than HbSS, clinical picture is of SCA, splenomegaly.
Hb C – lysine replaces GA at position 6
Hb D glutamine replaces GA
Hb E lysine replaces GA at position 26.

67
Q

Features of β-thalassaemia?

A

Loss of 1 βchain causes mild microcytic anaemia
Loss of both β⁰ = thalassaemia major
Excess α-chains ppt in erythroblasts = haemolysis + ineffective erythropoiesis

68
Q

Features of α-thalassaemia?

A

Loss of 1/2/3/4 α-chains:
1/2 = mild microcytic anaemia
3 = moderate anaemia - Hb H disease
4 = death in utero (hydrops fetalis)

69
Q

What do HbS C look like?

A

rhomboidal + spherocytic cells

70
Q

Why does 🔴 survival depend on cytoplasmic E in metabolic pathways?

A

unable to do oxidative phosphorylation + protein synthesis

71
Q

Role of cytoplasmic E?

A

maintain pliability of membrane,
maintain membrane transport of ions
keep the Hb iron in ferrous form not ferric form
prevent oxidation of proteins in 🔴

72
Q

Describe the process of pentose phosphate pathway

A
  • Glucose -> G6P
  • G6P -> 6PG by G6PD
  • produces NADPH
  • reduces glutathione (GSSH) -> GSH
  • (NADPH -> NADP)
  • GSH is anti-oxidant by conversion to GSSG + removes oxidants
  • Cycle restart (anti-oxidants reduced by excess alcohol consumption)
  • Pentose phosphate shunt provides NADPH maintaining GSH levels when GSSG formed
73
Q

How’s 10% of 🔴 glucose is metabolized?

A

Pentose Phosphate Pathway (Hexose Monophosphate Shunt HMS)

74
Q

Role of G6PD?

A

glucose-6phosphatedehydrogenase

catalyses G6P-> 6PG 1st step of pentose phosphate shunt producing NADPH

75
Q

Role of NADPH?

A

reduced nicotinamide adenine dinuclotide phosphate

  • protects 🔴 from oxidative damage
  • maintains GSH by reducing GSSH -> GSH
76
Q

Role of GSH?

A

reduced glutathione

  • anti-oxidant by removing oxidants to convert to GSSG
  • tripeptide protects Hb +🔴 membranes from oxidant stress from exposure to H2O2, medications, foods, infections
77
Q

Role of G6P?

A

glucose-6-phosphate

-converted to 6PG by G6PD producing NADPH

78
Q

Role of 6PG?

A

6-phosphogluconate

converted from G6P by G6PD producing NADPH

79
Q

What are heinz bodies?

A

when Hb ppt out due to oxidants

80
Q

What happens in G6PD def (enzymopathy)?

A

-No NADPH + GSH production:
Acute haemolysis when oxidant stress: oxidative drugs, fava beans, infections
Heinz bodies

81
Q

What’s G6PD def + benefit?

A 
enzymopathy
X-linked
occurs in same ethnic groups as haemoglobinopathies
affects 400M people
resistant to malaria
82
Q

Why’s the pyruvate kinase vital?

A

for glycolytic pathway which generates ATP to:

  • maintain 🔴shape + deformability
  • regulate intracellular cation conc via Na+/K+pump 3Na+out and 2K+in
83
Q

What happens in PK def?

A

No ATP:

  • cation pump failure - cells lose K+ + H2O
  • chronic non-spherocytic haemolytic anaemia
  • excess haemolysis = jaundice, gallstones
84
Q

How does normal haemolysis occur?

A

extravascularly in macrophages in spleen:
iron (recycled + binds to transferrin)
globin -> AA(recycled)
protoporphyrin-> unconjugated bilirubin (travels to liver,gets conjugated, excreted)

85
Q

How does abnormal haemolysis occur?

A

intravascularly (blood in urine)

CVS II (19 decks)

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