Red Blood Cells Flashcards
(212 cards)
1
Q
What are the main functions of Erythrocytes?
A
To transport oxygen to the tissues and remove carbon dioxide.
2
Q
Describe the cell membrane of erythrocytes.
A
Uncomplicated
3
Q
What are the advantages and disadvantages of the cell membrane of erythrocytes being uncomplicated ?
A
Ad = Simple passage of oxygen. Dis = Fragile so easily damaged.
4
Q
What are the advantages of RBCs lacking nucleuses and most cellular enzymes and organelles?
A
Ad = Flexibility to penetrate fine capillaries. Oxygen not used for ATP production.
Dis = Can’t make protective enzymes or maintain membrane integrity.
5
Q
What is the purpose of RBCs lacking HLA molecules?
A
Makes them easy to use in blood transfusion.
6
Q
What are HLA molecules and what is their overall purpose?
A
Human Leukocyte Antigen
Part of the immune system - aid immunity.
7
Q
What is the average lifespan of a red blood cell?
A
About 120 days.
8
Q
What causes the fluidity of the RBCs membrane?
A
A unique Cholesterol:Phospholipid ration.
9
Q
What enables red blood cells to uptake alot of glucose?
A
Many GLUT1’s - Glucose transporter 1 proteins.
10
Q
Draw a regular Bohr curve and then one of increased Carbon dioxide concentration.
A
In notes
11
Q
Draw a regular Haldane effect graph and then one with a higher concentration of oxygen present.
A
In notes
12
Q
What does the Haldane effect state?
A
The concentration of oxygen alters the affinity of haemoglobin to carbon dioxide and protons.
13
Q
What does the Bohr effect state?
A
Carbon dioxide and protons affect the affinity of haemoglobin to oxygen.
14
Q
How does increase oxygen affect the affinity of carbon dioxide to haemoglobin? (According to the Haldane effect). And what effect does this have?
A
Increased oxygen decreases the affinity of Hb to CO2 so more CO2 is delivered to the lungs.
15
Q
How does partial pressure of oxygen affect the affinity of haemoglobin to oxygen according to the Bohr effect? And what effect does this have?
A
If partial pressure of oxygen decreases, affinity of Hb to oxygen decreases so more oxygen is delivered to the respiring tissues.
16
Q
How does carbon dioxide affect the affinity of oxygen to haemoglobin according to the Bohr effect?
A
More carbon dioxide reduces the affinity of oxygen to haemoglobin.
17
Q
What happens to carbon dioxide in Red blood cells (starting with the use of carbonic anhydrase) and what effect does this have?
A
Carbon dioxide is hydrated to carbonic acid using carbonic anhydrase.
Carbonic acid spontaneously dissociates to form Hydrogen Carbonate ions and a hydrogen ion.
The decreased partial pressure of carbon dioxide in read blood cells causes more carbon dioxide to diffuse out of the cells.
18
Q
What is the formula for carbonic acid?
A
H2CO3
19
Q
What is the formula for hydrogen carbonate ions?
A
HCO3-
20
Q
What is the purpose of hydrogen carbonate ions in the blood?
A
Acts as a buffer
21
Q
Outline how hydrogen carbonate ions work as a buffer in the blood and what is required for this process.
A
Red blood cells exchange bicarbonate for chloride using the anion exchanged protein (band 3).
22
Q
What is the purpose of the chloride shift in red blood cells?
A
Maintain a carbon dioxide gradient so that carbon dioxide can diffuse out of the tissues and into the blood. This then decreases blood pH and causes oxygen to be released into the interstitial fluid.
23
Q
What is the chloride shift in the blood?
A
When red blood cells exchange bicarbonate for chloride using the anion exchanger protein (band 3).
24
Q
What happens to the red blood cells as the carbon dioxide diffuses across the alveolar membrane - in terms of carbonic acid etc.
A
Plasma carbon dioxide levels decrease.
Carbonic acid in the red blood cells is converted back into carbon dioxide and water by carbonic hydrase.
Bicarbonate moves back into the RBC’s in exchange for chloride.
25
Why is bicarbonate moved back into the red blood cells when carbon dioxide concentration in the blood decreases?
Replenishes the bicarbonate consumed by the hydrolysis reaction
26
Describe the shape of the oxygen dissociation curve.
Sigmodial - curved in 2 directionals like an S.
27
What is meant by a sigmoidal curve?
Curved in 2 directions like an S.
28
Why is the blood more alkaline in the lungs and how does this affect the oxygen dissociation curve?
Carbonic acid is lost.
| Curve shifts left
29
How does pH of the blood change in the lungs and why?
pH increases - more alkaline due to the loss of carbon acid.
30
If carbon dioxide diffuses from the capillaries, how does this affect the oxygen dissociation curve?
Shifts to the right
31
How does exercise affect blood pH and why?
Blood becomes more acidic due to presence of lactic acid.
32
When do reactive oxygen species form in the blood?
They are by-products of metabolism of oxygen.
33
How can reactive oxygen species damage cells?
Target fatty and amino acids in the cell membrane and denature them.
34
How do red blood cells protect themselves against reactive oxygen species in the blood?
They have a high concentration of anti-oxidants.
35
What is the main antioxidant used by red blood cells to protect themselves against reactive oxygen species?
Glutathione
36
How does Glutathione protect red blood cells from reactive oxygen species in the blood?
Donates hydrogen to oxygen molecules to produce water which is harmless. This means Glutatione can be converted back to glutaione reductase and NADH.
37
How many haemoglobin molecules does each red blood cell contain?
About 640 million
38
Describe the tertiary structure of haemoglobin and what function does this give?
4 polypeptide coiled chaines.
Hydrophobic R groups inside the molecule.
Hydrophilic R groups on the outside of the molecule - form hydrogen bonds with water molecules to allow solubility.
39
How many harm groups combine with 1 oxygen molecule?
1
40
How many oxygen molecules can combine with 1 haemoglobin molecule ?
4
41
When is the affinity of haemoglobin to oxygen high?
When there is a high concentration of oxygen in the tissues.
42
When is the affinity of haemoglobin to oxygen low?
When there is a low concentration of oxygen in the tissues.
43
How does it help when one molecule of oxygen binds to haemoglobin?
This causes the haemoglobin molecule to change shape so that it is easier for oxygen to combine with the other 3 haem groups.
44
What cell type removes ruptured red blood cells?
Macrophages
45
What happens to ruptured red blood cells after they have been removed by macrophages?
They are re-cycle
46
Why can't red blood cell s synthesise proteins for repair if they are damaged?
They have no nucleus or other organelles.
47
Where are erythrocytes produced?
Red bone marrow
48
What is it called when there is too much iron in the blood?
Hemochtomatosis
49
What is hemochrombtosis?
A hereditary condition where too much iron is absorbed into the blood from the foods being eaten. This excess iron accumulates in organs and compromises their functioning.
50
What is meant by the term Erythropoiesis?
Red blood cell formation.
51
How long does Erythropoiesis take?
2 wees
52
Wha stimulates the bone marrow to perform Erythropoiesis?
The kidneys releasing erythropoietin (EPO).
53
What stimulates the release of Thyroxine by the kidneys?
Testosterone
54
Why do men usually have more red blood cells than women?
Testosterone stimulates the release of Thyroxine which stimulates the release of EPO from the kidneys. This stimulated erythropoiesis (red blood cell formation).
55
What does erythropoietin do when it is released from the kidneys?
Stimulates Erythropoiesis in the red bone marrow
56
When is EPO released from the kidneys?
When blood volume is too low.
| When there is insufficient oxygen in the blood.
57
What is blood doping and when is it done?
Athletes take blood out of them then return it to their blood stream after 2 weeks. Increases oxygen carrying capacity of the blood.
58
What are the advantages and disadvantages of blood doping ?
```
Ad = increasing oxygen carrying capacity to increase stamina.
Dis = Increased risk of stroke.
```
59
Outline the process of Erythropoiesis.
Stem cells create burst forming units then colony forming units in the red bone marrow.
Large proerythrocytes are then formed which steadily shrink through successive cell division into erythroblasts, where haemoglobin synthesis begins.
Eventually they differentiate into reticulocytes which eject their nuclei and digest redundant organelles.
They pass into the blood and differentiate into red blood cells.
60
How long do reticulocytes last for in the body?
About 1 day
61
What happens if erythropoiesis can't keep up with red blood cell demand?
Hypoxia which can cause diseases such as anaemia or circulatory diseases.
62
Outline the process of erythropoietin signalling causing cell growth and maturation.
EPO binds to its receptor.
Phosphorylates JAK enzymes.
This causes EPO-R phosphorylation.
Second messenger (STAT) is phosphorylated.
Phosphorylated STAT travels to the nucleus of the cell and turns on growth promoting and maturing genes.
63
What is the main goal of erythropoietin signalling?
Causes cell growth and maturation
64
What are small red blood cells?
Red blood cells which are fewer in number and contain less haemoglobin.
65
What often causes small red blood cells?
Anaemia
66
What often causes large red blood cells?
Prolonged, excessive alcohol intake.
67
What is the proper name for small red blood cells?
Microcytic red blood cells
68
What is the proper name for large red blood cells?
Microcytic red blood cells
69
How does excessive alcohol consumption affect red blood cells?
Damages the red bone marrow and reduces vitamin B12 levels. Causes larger red blood cells to be produced meaning there isn't enough room for as many red blood cells and so haemoglobin concentration is reduced.
70
What is Spherocytosis?
Sphere-shaped red blood cells which are often jagged.
71
What causes Spherocytosis?
Mechanical destruction often red blood cells which is often due to thrombotic disorders.
72
What are hypo chromic red blood cells?
Red blood cells which are abnormally pale due to a lack of haemoglobin.
73
What is Echinocyte?
A reversible condition of red blood cells that is means artefacts are produced and act as coagulants therefore leading to blood clotting?
74
What is a coagulant?
Leads to clotting
75
What are the symptoms of severe anaemia?
Fainting, chest pain, angina, heart attacks
76
What is angina?
Chest pain caused by reduced blood flow to the heart.
77
What is the key cause of anaemia?
Lack of oxygen to the tissues meaning the cells can't efficiently generate ATP from glucose.
78
Name some causes of anaemia.
Iron imbalance, issues with the bone marrow, lack of vitamins, organ diseases, blood loss, gene mutations, haemolysis.
79
How can anaemia arises due to issues with the bone marrow generally?
Damage to the red bone marrow causes reduced red blood cell production = pure red cell aplasia.
80
What is pancytopenia?
Deficiency of red blood cells, white blood cells and platelets.
81
What is aplastic anaemia?
Insufficient new red blood cells are produced.
82
What are acquired factors which contribute to anaemia?
Infections such as hepatitis, alcohol, chemotherapy, solid tumours.
83
What is meant by the term idiopathic?
Spontaneously arriving disease
84
What is meant by the term congenital?
A disease present from birth.
85
What enzyme releases B12 vitamin and where does this occur?
Released by proteolysis in the acidic environment of the stomach.
86
What molecule is used to protect B12 vitamin from acid degradation and where is it produced?
Haptocorrin - salivary glands
87
What is the main source of B12 vitamin?
Meat and fish
88
What effect do the pH of the stomach and presence of haptocorrin have on B12 vitamin?
Allow it to bind to a gastric intrinsic factor.
89
What receptor types do B12 complexes bind to?
Cubam receptors
90
What happens when B12 complexes bind to cuban receptors?
Receptor-mediate endocytosis of B12 into the enterocytes of the distal ileum.
91
What causes B12 vitamin to exit the membrane of the enterocytes and what facilitates this process?
Lysosomal release
Facilitated by multi drug resistance protein 1
92
What is B12 an essential co-factor for?
Haemoglobin synthesis
93
What is one of the main causes of a lack of B12 vitamin?
Vegan diet
94
How does hepatitis lead to anaemia?
Inflammation of the lier means less iron is stored and synthesised.
95
How does chronic renal failure lead to anaemia?
Kidneys produce less erythropoietin for red blood cell production.
96
How do stomach ulcers, cancers and inflammatory bowl disease lead to anaemia?
Slowed absorption of iron and B12 into the intestines and stomach. Leads to blood loss.
97
What hormones are released from the pituitary that release red blood cell formation?
```
Gonodotropins
Adrenocorticotropic hormone (ACTH)
```
98
What are haemoglobinopathies?
Genetic disorders of haemoglobin. Cause altered structure or loss of haemoglobin.
99
What is sickle cell and what causes it?
Haemoglobin forms long, inflexible chains which means that blood cells are stiff and angular, causing them to become stuck in small capillaries.
100
Describe the dominance of sickle cell.
Autosomal recessive condition.
101
Define haemostasis
Stopping bleeding
102
Define thrombosis
The formation or presence of a blood clot in a blood vessel.
103
What are the key functions of Haemostasis?
Maintain blood within a fluid state in the blood vessels.
Stop bleeding after injury but maintain blood flow in the vessels.
Removal of the blood clot.
104
What is the Vasculature?
The arrangement of blood vessels in a specific organ or body part.
105
What are anticoagulants?
Prevent blood clots
106
What molecules are used to keep the blood in liquid form?
Anticoagulants
107
What are procoagulants?
Help form blood clots
108
Where are procoagulants released from and what do they enable?
From the damaged blood vessels after trauma.
| Enable primary and secondary haemostasis.
109
What is the dissolving of a blot clot called ?
Fibrinolysis
110
What is used by endothelial cells to inhibit the expression of adhesion molecules on platelets and endothelial cells?
Nitric Oxide and Prostoglandin
111
What are the purposes of Nitric Oxide and Prostoglandin to platelets and endothelial cells?
Inhibit expression of adhesion molecules on their surfaces.
112
What is used to protect the procoagulant of arteries?
Endothelial cells of the tunica initma.
113
What is the purpose of the endothelial cells of the tunica intima of arteries?
Protects the procoagulant underneath.
114
What is the purpose of the smooth muscle in arteries?
Allows contraction and relaxation
115
What are the purpose of alpha granules in platelets/
Contain adhesive proteins
116
What is the purpose of the surface connecting tubule on platelets?
Increases surface area.
117
Where is fibrinogen found in the blood?
Plasma
118
What does platelet plug formation require to begin?
Exposure to extracellular matrix proteins.
119
Where is collagen in platelets?
Extracellular matrix
120
What are the steps of platelet plug formation?
Platelet adhesion
Platelet activation and secretion
Platelet plug formation
121
What substance is the main activator of platelet plug formation and where is it found?
Tissue Factor
| Found as a membrane bound protein expressed on many cells but not in the blood.
122
What causes the extrinsic coagulation platelet plug formation model?
Damage to tissue outside the vessel
123
What causes the intrinsic coagulation platelet plug formation model?
Damage to the blood vessel
124
Compare the speed of the intrinsic and extrinsic platelet plug formation models.
```
Extrinsic = Rapid
Intrinsic = Slower because more complex.
```
125
What is used to break the blood clot when it is no longer needed?
Fibrinogen is used to do fibrinolysis of the platelet plug.
Tissue plasminogen activator - binds to plasminogen on clots and activates them into plasmin. This dissolves the clot.
126
What is secondary haemostasis and what causes this to occur?
The coagulation cascade.
| Caused by a large trauma.
127
What is primary haemostasis and what causes this to occur?
Temporary platelet plug formation due to small trauma.
128
Describe what activates platelet plug formation.
The normal, intact endothelium is damaged by trauma. Therefore exposing the sub-endothelium collagen to Tissue Factors. Tissue factors activate the localised clotting mechanisms.
Platelets swell and form Pseudopods.
129
What is Tissue Factor used for in platelet plug formation?
It is used to activate a localised clotting mechanism at the site of injury.
130
How does the step of adherence occur in the platelet plug formation process?
The platelet pseudopods have GP1b on their glycoprotein membrane. This binds to VWF on the sub-endothelial collagen.
131
What happens when a platelet pseudopod binds to the sub-endothelial collagen during platelet plug formation?
Platelets Swell.
Platelets contract.
Platelets release granules.
132
What granules do the platelets release when they contract during plug formation?
ADP, VWF and Thrmobin
133
What happens when ADP is released from a platelet during plug formation?
ADP activates GP2b/3a receptors on the platelet surface to have a conformational change and therefore be present in their active form.
It also causes other platelets to move to the site of injury.
134
How does ADP activate G2b/3a receptors on platelet surfaces?
ADP activates P2Y1 and P2Y12 receptors on the platelets. This causes a conformational change in the G2b/3a receptors and causes then to move from their inactive form to their active forms.
135
What causes thrombin A2 to be released from the platelets?
Platelet contraction
136
What does the release of Thrmobin A2 from platelets cause?
Platelet aggregation
Vasoconstriction
Bronchoconstriction
137
How does platelet aggregation occur one the G2b/3a receptors have been activated in the plug formation process?
The G2b/3a receptors on platelet molecules bind with a fibrinogen molecule in the middle of them.
138
How does secondary haemostasis occur once the G2b/3a receptors have banded during platelet plug formation?
Thrombin and platelet factor 3 is used to convert the fibrinogen molecule between the receptors into a very strong meshwork of fibrin. This creates strong platelet adhesion.
139
What is the purpose of platelet factor 3 during platelet plug formation?
It allows fibrinogen to be converted to fibrin meshwork to create strong adhesion between platelet molecules ad continue the coagulation cascade.
140
How does the fibrin meshwork between platelets allow a blood clot to form?
It traps red blood cells and prevents bleeding.
141
What are zymogens and where are they activated?
Inactive substances which are activated by enzymes and are often peptidases.
Activated on cell membrane.
142
What is thrombocytopenia ?
Platelet count below 50,000
143
What is thrombocytosis?
Platelet count greater than 750,000
144
What cells synthesise platelets?
Megakaryocytes
145
Outline how platelets are formed.
Megakaryocytes are produced in the bone marrow. They then squeeze through the capillaries and break into thousands of platelet pieces as they do so.
146
What is thrombocytopenia?
A platelet count below 50,000
147
What is thrombocytosis?
A platelet count above 750,000
148
Why are platelets not classified as cells?
They have no nucleus and no ability to divide.
149
Can platelets be seen by bone marrow biopsy?
No - only the megakaryocytes can be seen.
150
What test is needed to be able to see platelets?
Blood smear
151
Where are platelets usually found in the body?
Peripheral blood
| Spleen
152
What is peripheral blood?
Blood which is circulating and not sequestered in the spleen, lymphatic system, liver or bone marrow.
153
What is splenomegaly?
Decreased blood count due to the spleen being enlarged and trapping too many platelets. This clogs the spleen and can affect its functioning.
Also leads to thrombocytopenia.
154
What are the boundaries thrombocytopenia when caused by the spleen?
A low blood count but never less than 40,000 per microlitre.
155
How is thrombocytopenia treated when caused by splenomegaly and how does this work?
Remove the spleen by splenectomy. This means that the platelets are no longer hidden by the enlarged spleen and are therefore forced into the bloodstream. This increases the platelet count in the blood.
156
How do we know if thrombocytopenia is not caused by the spleen?
If the platelet count is below 20,000 per micro litre of blood, the issue is not caused by the spleen.
157
What chemicals stimulate platelet production?
Thrombopoietin
| Interleuken - 6
158
Where is the chemical throbopoietin produced?
Liver
159
How does Interleuken-6 sometimes lead to thrombocytosis?
Stimulates the release of thrombopoietin meaning more platelet production is stimulated. Excessive platelets in the blood causes thrombocytosis.
160
How long do platelets last in the blood stream?
Between 8 and 12 days.
161
What cells remove platelets from the blood stream?
Splenic macrophages.
162
What is the overall shape of platelets and what do they consist of?
Biconvex pieces of megakaryocytic plasma membrane and cytoplasm.
163
What does the plasma membrane of platelets consist of?
Phospholipids and arachiondic acid
164
What covers the plasma membrane of platelets?
Glycoprotein
165
What is the purpose of the glycoproteins covering platelets?
Stores G2b/3a and GP1b receptors for platelet plug formation.
166
What is the purpose of Ca2+ in platelet plasma membrane?
Contraction of platelets and release of granules
167
Where is Ca2+ found in platelets?
Plasma membrane and cytoplasm
168
What proteins make up the cytoplasm of platelets?
Actin, Myosin and Thrombosthenin
169
What is the purpose of actin, myosin and thrombosthenin in the cytoplasm of platelets?
Allows contraction of platelets to release granules.
170
What allows protein synthesis in platelets?
Residuals of Golgi apparatus and RER
171
Why do platelets have many mitochondria in their cytoplasm?
For ADP and ATP production.
172
What is the stabilising factor in the cytoplasm of platelets?
Fibrin
173
What is the purpose of Platelet delivered growth factors in the cytoplasm of platelets?
Repair vessels of thrombosis
174
Where are platelet derived growth factors found in platelets?
Cytoplasm
175
Where are granules found in platelets?
Cytoplasm
176
What are the granule types in platelets?
Alpha
| Dese
177
What type of molecule are the alpha granules in proteins?
Mnemonic proteins
178
What are Mnemonic proteins?
Have memory functions.
179
What is contained within the alpha granules of platelets?
Factor XIII, Platelet activating factor (PAF), Platelet derived growth factor (PDGF), Von Willerband factor (VWF), Platelet factor 4 (PF4).
180
What is the purpose of Factor XIII in the alpha granules of platelets?
Fibrin stabilising factor.
181
Are dense and alpha granules found in platelets protein molecules?
Alpha - yes
| Dense - no
182
What do dense granules of platelets contain?
ADP and Ca2+
183
What is the purpose of Ca2+ in the dense granules of platelets?
Contraction of the platelets.
| Binding agent for vitamin k dependent factors
184
Compare the possible pathways of the cascade and cell based models for blood coagulation.
Cascade - intrinsic and extrinsic work independently and meet at a common end-point
Cell based - extrinsic pathway only
185
Compare the main factors that the cascade and cell based models rely on to form blood clots.
Cascade - Generate large amounts of thrombin to form clots.
Cell based - Works on platelets to produce the thrombi burst.
186
What factor does the cell based model of blood coagulation lack that the cascade model requires?
Factor XIII
187
Compare what controls the coagulation process in the cascade and cell based models.
Cascade - coagulation factors control the rate.
| Cell based - platelets and endothelial cells control rate.
188
What does secondary homeostasis have to have to continue?
Clotting factors
189
How long does secondary homeostasis take to form blood clots?
Few minutes
190
What are the 3 pathways of secondary hemostasis?
Extrinsic
Intrinsic
Common
191
Outline the extrinsic secondary hemostasis pathway.
In notes
192
Outline the intrinsic secondary hemostasis pathway.
In notes
193
Outline the common secondary hemostasis pathway.
In notes
194
What is haemophilia?
Reduction in the ability to form blood clots.
195
What is primary hemostasis?
Platelet plug formation.
196
What is secondary hemostasis?
Coagulation cascase
197
Name some symptoms of haemophilia.
```
Easy bruising
Hematomas
Prolonged bleeding
Gastrointestinal bleeding
Hematuria
Hemathrosis
Bleeding into the joints.
```
198
What are hematomas?
Collection of blood outside the vessels (often in the muscles).
199
What is hematuria?
Blood in the urine
200
What is hemathrosis?
Bleeding into the joint spaces.
201
What lab tests can be used to diagnose haemophilia and how do they work?
Prothrombin time = looks at extrinsic and common pathways.
Partial thromabtic time = looks at intrinsic and common pathways.
If both tests are slow - indicates issues in common pathway.
Can also do tests on platelets, specific factor activities and looking for mutations.
202
How can haemophilia be treated?
Injections of missing or nonfictional co-factors.
| Desmopressin
203
What is desmopressing and how is it used to treat haemophilia?
It helps with mild VIII cofactor deficiency by stimulating vWF release and therefore stimulation the quantity of VIII.
204
Which mediations may people with haemophilia be told not to take?
Aspirin
205
How may issues with the common pathway of hematosis be found?
Slow prothrombin time and partial thrombotic time.
206
When would you expect to see progenitor cells in he peripheral blood stream?
Indicates forms of metastatic cancer.
207
What tests are used to identify anaemia?
Blood smear
| Full blood count
208
What does. blood film show?
Identify anaemias, look at red and white blood cells (count and shape).
209
Why do some people have anaemia and not show symptoms?
Mild, slow onset, age, well adapted.
210
Why would it be helpful to look at the number of reticulocytes in the blood?
To see whether the red cells are healthy or not. Can help diagnose anaemia.
211
What are reticulocytes?
Immature red blood cells which are granulated.
212
Why are serum ferrin tests often inaccurate?
They are highly sensitive and non-specific.
