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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
What are the coagulation factors in haemostasis?
- 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
26
the Clot cascade
Extrinisic and intrinsic pathways lead to common pathways which lead to the clot
27
What is The common pathway?
- how the fibrin clot is made | - must be initiated by the extrinsic pathway
28
What is Serum?
- fluid left after clotting | - missing fibrinogen, clotting factors II, V, VII
29
give an overview of Coagulation starting from fibrinogen
- a positive feedback loop | fibrinogen --(thrombin)--> fibrin--(XIII + Ca2+) --> fribrin cross-linked, a stable clot
30
Two coagulation cascades
- Extrinisce (tissue factor) pathway | - Intrinsic (contact activation) pathway
31
Explain the activation of Thrombin, including the appropriate factors
- poorly activated by Factor Xa - cofactor Va makes it more effective - factor X needs to be activated
32
Explain the three pathways to activate Factor Xa
- Extrinsic Xase - Intrinsic Xase - Thrombin also activates it (positive feedback)
33
What makes up the Extrinsic Xase?
- Tissue factor + factor VIIa
34
What is Intrinsic Xase?
- Factor VIIIa + Factor IXa
35
What are the Prothrombin group coagulation factors?
Factors; - II - VII - IX - X
36
What are the Thrombin group coagulation factors
Factors: - I - V - VIII
37
what is the importance of Vitamin K in coagulation
- 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
What is Plasmin
- lyses of fibrin - starts as inactive plasminogen - requires tissue plasminogen activator to mature
39
What is Protein C and what is its action?
- Coagulation Inhibitor - starts as an inactive enzyme - inactivates Factor Va & Factor VIIIa, by working with co-facto Protein S
40
What is Antithrombin III? | - where, what, how
- 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
What is the cause and result of Vitamin K deficiency?
- 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
What is Haemophilia A and how is it treated?
- clotting disorder, affects larger vessels, joints, muscles - due to congenital lack of factor VIII - X-linked disease - Treat with injected purified Factor VIII
43
Haemophilia B, Christmas disease
- defect is factor IX | - similar symptoms of haemophilia A
44
Explain how Atherogenesis can present as a disease inflammation
- monocytes enter lesion -> become macrophages - these become foam cells - these cells die and release their contents attracting more - monocytes, - cytokines - chemo-attractants
45
Explain how Atherogeniss can present as a lipid disease
- 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
Explain how Atherogenesis presents as an endothelium disease
- endothelium express chemoattractants - when endothelium is lost collagens stimulates coagulation - when endothelium is lost, vessel cannot control its dilation
47
Pharmocological control of blood clots
- Anti platelets agents - Anticoagulent - Firbinolytics
48
What do Anti-platelet Agents do, give an example
- prevents clotting in arteries - Aspirin - ADP receptor inhibitors, Prasugrel/Clopidogrel
49
what do Anticoagulants do, give examples
- preventing clotting in veins, prevents, fibrin-mesh - Heparins - Novel Oral Anti-coagulants - Warfarin
50
what is the action of Fibrinoltyics, give an example
- clotting in arteries with a high pressure - example is Tissue Plasminogen Activator - Streptokinase - Urokinase
51
What is the difference between an erythrocyte (1), a reticulocyte (2), and a blast forming cell (3)?
- (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
What are the stages of erythropoiesis in terms of cell division and development
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
Name the cells that arise from the lymphoid progenitors and those that arise from the myeloid progenitors
- 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
What are the normal female values for the PCV, MCH, blood Hb, and MCV?
- PCV (haematocrit): 36-48% - MCH (Mean Hb): 12-16g/dL - blood Hb: 27-34pg - MCV: 80-100fL
55
What are the normal male values for the PCV, MCH, blood Hb, and MCV?
- PCV (haematocrit): 40-52% - MCH: 13-17 g/dL - blood Hb: 27-34pg - MCV: 80-100fL
56
What are the differences between myoglobin, foetal and maternal haemoglobin
- 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
What is methaemoglobinemia?
- the Fe in Hb is oxidized (Fe3+ instead of Fe2+) | - Cannot transport O2, does not release O2 into the tissue
58
What is the cause of methaemoglobinanemia?
- 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
What are the symptoms and complications of polycythaemia?
- Increased haematocrit (PVC- no. of RBC) - increased blood viscosity, clogged blood vessels --> erythrocytosis - physiological poly.: due to living at high altitude
60
What are the symptoms and complications of polycythaemia vera?
- often asymptomatic - risk of thrombotic events - no, cure, vensection - occurs in all ages increase with age
61
When would polycythaemia bot be considered pathological?
- if there was a need for it, such as living in a high altitude
62
Iron depletion results in what type of anemia?
hypochromic microcytic anaemia | - the cells keep dividing but they don't fill up with Hb
63
Vitamin B12 /Folic acid depletion leads to what type of anemia?
megaloblastic macrocytic anaemia | - the cells keep filling up but they cannot divide fast enough
64
Why don't erythrocytes have microvilli
- 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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