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103: Theme 2 > Red Blood Cell Physiology > Flashcards

Red Blood Cell Physiology Flashcards

1
Q

what is Myoglobin ?

A

an oxygen binding unit found in myocytes

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2
Q

Haem group structure

A
  • porphyrin ring, that gives the red colour

- Fe2+ ferrous ion

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3
Q

Maternal Haemoglobin

A

HbA

  • 2x alpha haemoglobin
  • 2x beta haemoglobin
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4
Q

Foetal Haemoglobin

A

HbF

  • 2x alpha haemoglobin
  • 2x gamma haemoglobin
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5
Q

what are the 3 transport mechanisms of CO2

A
  • 10 % dissolved
  • 22% as carbamino, forms a carboxyl group
  • 68% as HCO3-
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6
Q

Explain CO2 transport as HCO3-, via the chloride shift

A
  • inside the celll CO2 + H2O = H2CO3 H+ HCO3-
  • the HCO3- is exchanged with Cl- from outside the cell
  • increasing the overl CL- concentration in the cell
  • H+ + Hb- = HHb
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7
Q

What is 2,3-DPG

A

2,3 diphosphoglycerate

- binds to Hb

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8
Q

Action of 2,3-DPG

A
  • lowers affinity Hb to O2
  • found in erythrocytes at 5mM
  • HbF as lower affinity than HbA, therefore has a higher affinity for oxygen than HbA
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9
Q

How is breathing controlled by CO2, O2 and H+

A
  • plasma O2 must be below 88% to increase the respiratory drive
  • H+ in the CSF is the main drive
  • CO2 in the blood is related to control from the carotid arch
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10
Q

Describe Erythrocytes

A
  • transport CO2 and O2
  • survive 120 days
  • biconcave
  • anucleate, no organelles
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11
Q

What is the Haemotocrit

A

the packed cell volume, if it where to be centrifuged

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12
Q

What is the Female Haematocrit?

A

36-48%

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13
Q

What is the Male Haematocrit?

A

40-52%

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14
Q

Carbamino Hb equation

A

CO2 + Hb-(H)2 HB-N(H)(COOH)

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15
Q

What is the action of Endothelial cells ?

A
  • control blood fluidity and flow
  • signals inflammatory cells to areas needing defence/repair
  • partially permeable barrier between blood and tissue
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16
Q

What is the von Willebrand factor

A

a blood protein that is important for triggering various aspects of clotting

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17
Q

What are the 3 platelet-based pathways to repair blood vessels

A
  • Platelets
  • coagulation
  • vasoconstriction
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18
Q

What is the name used to encompass the risk factors for a haemostatic repair?
- what are these risk factors?

A

Virchow’s triad

  • Stasis of blood flow
  • Endothelial Injury
  • Hypercoagulability
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19
Q

How does vasoconstriction occur in Haemostasis

A 
- platelets release vasoconstrictive and pro-thrombotic factors
these cause vasoconstriction
- Serotonin
- ADP
- Thromboxane A2
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20
Q

Define Thrombocytopenia

A

low platelet count in the blood

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21
Q

what are Megakaryocytes

A

found in the bone marrow

- precursors to platlets

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22
Q

How are platelets activated for haemostasis

A 
- Platelet Activation = exocytose +
change shape + increased respiratory rate
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23
Q

What are the three A’s that lead to platelets acting as a haemostatic plug?

A
  • Adhesion to exposed collagen
  • Activation, exocytosis of dense granules by serotonin ADP and calcium
  • Aggregation, stimulated by ADP, blocked by Prasgruel
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24
Q

What is Prasugrel, how does it work?

A
  • anti-plaetlet drug
    works as an
  • antagonist of inhibitor of P2Y12ADP receptors
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25
Q

What are the coagulation factors in haemostasis?

A
  • clotting Factor Xa(active), enzyme
  • Factor V and VIII are not enzymes, act as co-factors
  • Initial activating factors are separated i.e tissue factors
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26
Q

the Clot cascade

A

Extrinisic and intrinsic pathways lead to common pathways which lead to the clot

27
Q

What is The common pathway?

A
  • how the fibrin clot is made

- must be initiated by the extrinsic pathway

28
Q

What is Serum?

A
  • fluid left after clotting

- missing fibrinogen, clotting factors II, V, VII

29
Q

give an overview of Coagulation starting from fibrinogen

A
  • a positive feedback loop

fibrinogen –(thrombin)–> fibrin–(XIII + Ca2+) –> fribrin cross-linked, a stable clot

30
Q

Two coagulation cascades

A
  • Extrinisce (tissue factor) pathway

- Intrinsic (contact activation) pathway

31
Q

Explain the activation of Thrombin, including the appropriate factors

A
  • poorly activated by Factor Xa
  • cofactor Va makes it more effective
  • factor X needs to be activated
32
Q

Explain the three pathways to activate Factor Xa

A
  • Extrinsic Xase
  • Intrinsic Xase
  • Thrombin also activates it (positive feedback)
33
Q

What makes up the Extrinsic Xase?

A
  • Tissue factor + factor VIIa
34
Q

What is Intrinsic Xase?

A
  • Factor VIIIa + Factor IXa
35
Q

What are the Prothrombin group coagulation factors?

A

Factors;

  • II
  • VII
  • IX
  • X
36
Q

What are the Thrombin group coagulation factors

A

Factors:

  • I
  • V
  • VIII
37
Q

what is the importance of Vitamin K in coagulation

A
  • clotting factors made by the liver, vitamin K is important to maintaining the liver
  • fat-soluble vitamin
  • synthesize enzyme coagulation factors
  • Prothrombin(II), VII, IX, X
  • gamma carboxylation of clotting enzymes
38
Q

What is Plasmin

A
  • lyses of fibrin
  • starts as inactive plasminogen
  • requires tissue plasminogen activator to mature
39
Q

What is Protein C and what is its action?

A
  • Coagulation Inhibitor
  • starts as an inactive enzyme
  • inactivates Factor Va & Factor VIIIa, by working with co-facto Protein S
40
Q

What is Antithrombin III?

- where, what, how

A
  • peptide formed in the liver
  • blocks activity of thrombin and Xa, IXa
  • activity increased by Heparin
  • AT III defieincy leads to thrombotic disease (too many clots)
  • can be formed recombinantly
41
Q

What is the cause and result of Vitamin K deficiency?

A
  • this is rare as vitamin K is made by bacteria of large intestine (leafy green vegetables)
  • caused by GI disease or no fact absorption
  • Warfarin prevents recycling of vitamin K
42
Q

What is Haemophilia A and how is it treated?

A
  • clotting disorder, affects larger vessels, joints, muscles
  • due to congenital lack of factor VIII
  • X-linked disease
  • Treat with injected purified Factor VIII
43
Q

Haemophilia B, Christmas disease

A
  • defect is factor IX

- similar symptoms of haemophilia A

44
Q

Explain how Atherogenesis can present as a disease inflammation

A
  • monocytes enter lesion -> become macrophages
  • these become foam cells
  • these cells die and release their contents attracting more
    • monocytes,
    • cytokines
    • chemo-attractants
45
Q

Explain how Atherogeniss can present as a lipid disease

A
  • lDL deposits lipids in lesion
  • cholesterol esters are non-aqueous
  • cholesterol esters are oxidized, making oxygen radicals which are immunogenic
  • oxidized lipids are consumed by macrophages, become foam cells…
  • foam cells eventually die and attract other factors leading to atherogenic plaque formation
46
Q

Explain how Atherogenesis presents as an endothelium disease

A
  • endothelium express chemoattractants
  • when endothelium is lost collagens stimulates coagulation
  • when endothelium is lost, vessel cannot control its dilation
47
Q

Pharmocological control of blood clots

A
  • Anti platelets agents
  • Anticoagulent
  • Firbinolytics
48
Q

What do Anti-platelet Agents do, give an example

A
  • prevents clotting in arteries
  • Aspirin
  • ADP receptor inhibitors, Prasugrel/Clopidogrel
49
Q

what do Anticoagulants do, give examples

A
  • preventing clotting in veins, prevents, fibrin-mesh
  • Heparins
  • Novel Oral Anti-coagulants
  • Warfarin
50
Q

what is the action of Fibrinoltyics, give an example

A
  • clotting in arteries with a high pressure
  • example is Tissue Plasminogen Activator
  • Streptokinase
  • Urokinase
51
Q

What is the difference between an erythrocyte (1), a reticulocyte (2), and a blast forming cell (3)?

A
  • (1) to (3) gets larger
  • (1) is a nucleate, (2) has a non functioning nucleus, (3) functioning nucleus
  • (3) is still a dividing cell, (1) and (2) have stopped dividing
52
Q

What are the stages of erythropoiesis in terms of cell division and development

A

stem cell –myeloid pathway–> blast forming cell —> colony forming unit —> pronormoblast (partially committed)

  • divides and becomes smaller, losing it’s nucleus
  • from a normoblast to a late normoblast –> reticulocyte –> RBC
53
Q

Name the cells that arise from the lymphoid progenitors and those that arise from the myeloid progenitors

A
  • T cells, B cells from lymphoid
  • Neutrophils, basophils/mast cell, eosinophils, monocytes/macrophages, megakaryocytes/platelets, erythrocytes
  • macrophages and neutrophils are both primary phagocytes, have a common precursor
54
Q

What are the normal female values for the PCV, MCH, blood Hb, and MCV?

A
  • PCV (haematocrit): 36-48%
  • MCH (Mean Hb): 12-16g/dL
  • blood Hb: 27-34pg
  • MCV: 80-100fL
55
Q

What are the normal male values for the PCV, MCH, blood Hb, and MCV?

A
  • PCV (haematocrit): 40-52%
  • MCH: 13-17 g/dL
  • blood Hb: 27-34pg
  • MCV: 80-100fL
56
Q

What are the differences between myoglobin, foetal and maternal haemoglobin

A
  • myoglobin has a really high affinity for oxygen, HbF and HbA are lower
  • HbF is slightly more left shifted, HbA is very right shifted
57
Q

What is methaemoglobinemia?

A
  • the Fe in Hb is oxidized (Fe3+ instead of Fe2+)

- Cannot transport O2, does not release O2 into the tissue

58
Q

What is the cause of methaemoglobinanemia?

A
  • congenital/ acquired globin mutations
  • Higher than normal Methoglobin being produced
  • MetHb not able to release O2 as effectively into body tissue
  • Hereditary through Cyt b5 reductase mutation
  • Type 1 the RBC doesn’t make this enzyme or type 2 when the enzyme doesn’t function
  • Acquired MetHb: medicines and chemicals cause it
  • i.e, anaesthetics, Nitrobenzens, antibiotics like chloroquine dapsone, Nitrites (additive in meat)
59
Q

What are the symptoms and complications of polycythaemia?

A
  • Increased haematocrit (PVC- no. of RBC)
  • increased blood viscosity, clogged blood vessels –> erythrocytosis
  • physiological poly.: due to living at high altitude
60
Q

What are the symptoms and complications of polycythaemia vera?

A
  • often asymptomatic
  • risk of thrombotic events
  • no, cure, vensection
  • occurs in all ages increase with age
61
Q

When would polycythaemia bot be considered pathological?

A
  • if there was a need for it, such as living in a high altitude
62
Q

Iron depletion results in what type of anemia?

A

hypochromic microcytic anaemia

- the cells keep dividing but they don’t fill up with Hb

63
Q

Vitamin B12 /Folic acid depletion leads to what type of anemia?

A

megaloblastic macrocytic anaemia

- the cells keep filling up but they cannot divide fast enough

64
Q

Why don’t erythrocytes have microvilli

A
  • would be ripped away by shearing forces of going though blood at high velocity
    cell would not be able to maintain repair of itself as there is no nucleus

103: Theme 2 (8 decks)

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