Physiology Flashcards

(115 cards)

1
Q

What are the 3 types of blood cells

A

Red blood cells
White blood cells
Platelets

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2
Q

Haematopoiesis

A

The production of blood cells

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3
Q

Haematopoiesis in the embryo

A

Yolk sac , then liver , then marrow

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4
Q

When do blood cells start to be produced in the spleen in an embryo

A

3rd - 7th month

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5
Q

Where are blood cells produced at birth

A

Mostly bone marrow

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6
Q

Where are blood cells produced during childhood

A

Bone marrow

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7
Q

Where are blood cells produced in an adult

A

Restricted to skull, ribs, sternum, pelvis and proximal ends of the femur

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8
Q

State the 3 types of white blood cells

A

Granulocytes
Monocytes
Lymphocytes

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9
Q

Name the 3 types of granulocytes

A

Neutrophils
Eosinophils
Basophils

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10
Q

What do neutrophils look like

A

Segmented nucleus , stains neutral

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11
Q

4 ways to assess haemopoeisis

A
  • peripheral blood (blood count and film)
  • bone marrow
  • immunophenotyping
  • other signs e.g. splenomegaly, hepatomegaly
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12
Q

Where is bone marrow usually taken from

A

Posterior iliac crests

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13
Q

Which 2 key organelles do red blood cells not have

A

Nucleus and mitochondria

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14
Q

What maintains water balance in red blood cells

A

Sodium-potassium pump

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15
Q

Structure of haemoglobin in most adults

A

2 alpha chains and 2 beta chains

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16
Q

Structure of foetal haemoglobin

A

2 alpha chains and 2 gamma chains

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17
Q

Structure of haemoglobin in HbA2

A

2 alpha chains 2 delta chains

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18
Q

How many oxygen molecules can bind to one haemoglobin

A

4

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19
Q

State 3 functions of haemoglobin

A
  • delivers oxygen to tissues
  • acts as a buffer for H+
  • CO2 transport
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20
Q

Erythropoiesis

A

Red cell production

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21
Q

Where does erythropoesis occur

A

Bone marrow

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22
Q

What regulates erythropoiesis

A

Erythropoietin

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23
Q

Where is erythropoietin found

A

In the kidneys

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24
Q

On which chromosome are alpha like genes found

A

16

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25
How many alpha genes do we have per chromosome
2
26
On which chromosome are beta like genes found
11
27
Where does RBC destruction usually occur
Spleen and liver
28
What is the haem group broke down to
Iron and bilirubin
29
What is metHb
Hb with Fe3+ instead of Fe2+
30
Embden-Meyerhof pathway
Red blood cells are able to generate ATP and NADH through the glycolysis pathway
31
What can cause an oxygen dissociation curve to the right (3)
2,3-DPG Low pH Increased temperature
32
What is the main role of iron in the body
Crucial for reversible oxygen binding to haemoglobin
33
Name 3 biological components in which iron is present
- haemoglobin - myoglobin - enzymes
34
What is a potential risk associated with iron due to its chemical reactivity
Can lead to oxidative stress and the production of free radicals
35
Where does iron absorption occur
Duodenum
36
What enhances iron absorption (3)
- haem vs non-haem iron - ascorbic acid - alcohol
37
What inhibits iron absorption (3)
- calcium - tannins (e.g. tea) - phylates
38
Where are phylates found in the diet
Cereals, bran, nuts, seeds
39
What is the main regulator of iron uptake
Hepcidin
40
When and where is hepcidin produced
In the liver in response to increase iron load and inflammation
41
Role of ferroportin
Facilitates iron export from the duodenal enterocyte
42
What transports iron around the body
Trasferrin
43
Role of hepcidin
Binds to ferroportin and causes its degradation
44
Where are lots of transferrin receptors found
Erythrocytes marrow
45
What does low ferritin suggest
Iron deficiency
46
How do we assess functional iron
Haemoglobin concentration
47
How do we assess transport iron
% saturation of transferrin with iron
48
How do we assess storage iron
Serum ferritin
49
Haemostasis
The arrest of bleeding and the maintenance of vascular patency
50
State the 4 components of a normal haemostatic system
- formation of a platelet plug - formation of fibrin clot - fibrinolysis - anticoagulant defences
51
Primary haemostasis
Formation of a platelet plug
52
Secondary haemostasis
Formation of a fibrin clot
53
How and where are platelets formed
In the marrow by budding from Megakaryocytes
54
Formation of a platelet plug (4)
- endothelial wall damage - exposes collagen and releases von willebrand factor - secretion of chemicals from the platelets - aggregation at the site of injury
55
State the 3 causes of failure of the platelet plug formation
- vascular - platelets - Von Willebrand factor deficiency
56
Vascular causes of failure of the platelet plug formation (3)
- Marfans - vasculitis - vit C deficiency
57
Consequences of failure of platelet plug formation (4)
- easy bruising - mucosal bleeding - intercranial haemorrhage - retinal haemorrhage
58
Screening test for primary haemostasis
Platelet count
59
Causes of failure of fibrin clot formation (4)
- single clotting factor deficiency - liver failure - vit K deficiency - increased fibrinolysis
60
Test which identifies failure in the extrinsic pathway
prothrombin time
61
Test which identifies failure in the intrinsic pathway
Activated partial thromboplastin time
62
Lifespan of a RBC
120 days
63
Lifespan of a neutrophil
7-8 hours
64
Lifespan of platelets
7-10 days
65
What are blasts
Nucleated precursor cells
66
Megakaryocytes
Platelet precursor
67
Myelocytes
Nucleated precursor between neutrophils and myeloblasts
68
Reticulocyte
Immature red blood cells
69
What is proliferation
Increase in numbers
70
Where do haemopoietic stem cells originate embryonically
Mesoderm
71
How are mature blood cells released from the bone marrow
Pass through fenestrations in endothelial cells of the sinusoids
72
What is the release of RBCs from the marrow associated with
Sinusoidal dilation and increased blood flow
73
Difference between red and yellow marrow
Red is active, yellow is fatty and inactive
74
What regulates neutrophil precursor maturation
G-CSF
75
What is the role of thrombopoietin
Regulates the growth and development of Megakaryocytes from their precursors
76
What are lymphatic channels
Blind ended vessels that permit passive unidirectional flow of lymphatic fluid
77
Role of the lymphatic system
Prevents oedema by returning fluid from extracellular connective tissues to the circulation
78
What are the 3 important regions of a lymph node
Cortex Paracortex Medulla
79
Cortex of a lymph node
Nodules of B lymphocytes arranged in follicles
80
Paracortex of a lymph node
Mainly T lymphocytes Forms interfollicular tissue which surrounds follicles and extends out and merges with medulla
81
Medulla of a lymph node
Contains cords and sinuses draining into the hilum
82
What happens in the dark zone of a lymphoid follicle
Clonal expansion and somatic hypermutation
83
What happens in somatic hypermutation
The DNA of B cells undergoes random mutations leading to changes in the antibody genes
84
What happens in the light zone of a lymphoid follicle
B cell selection and affinity maturation
85
How do B cells move from the dark zone to light zone
Increased antigen affinity
86
What happens to positively selected B cells in the light zone
Re enter dark zone and keep proliferating Differentiate into plasma cells Differentiate into memory B cells
87
Role of follicular dendritic cells (3)
provide architectural support to Germinal centre Facilitates debris removal through secreting bridging factor Role in antigen capture for memory B cells
88
What is a centroblast
Proliferating B cell in the dark zone
89
What is a Centrocyte
Differentiated centroblast B cell in the light zone
90
Flow of lymphatics (5)
Afferent channels drain lymph through the capsule into the subscapular sinus Percolates through the node Enters medullary cords and sinuses Sinuses merge at hilum and form efferent lymphatics Lymph rejoins extranodal circulation
91
Troiseries sign
Manifestation of metastasis from an abdominal malignancy
92
Sentinel lymph node
The first lymph node to which cancer cells are likely to spread
93
2 characteristics of malignant haemopoiesis
Increased numbers of abnormal and dysfunctional cells Loss of normal activity
94
What are the causes of abnormal haemopoiesis in malignancy
Increased proliferation in the absence of a stimulus Lack of differentiation Lack of maturation
95
Molecular pathogenesis in acute leukaemia
Proliferation of abnormal progenitors with a block in differentiation and maturation
96
Molecular pathogenesis in chronic myeloproliferative disorders
Proliferation of abnormal progenitors but no differentiation or maturation block
97
What are clones
Population of cells derived from a single parent cell
98
What are the 3 main ways we can class haematological malignancies
Lineage Developmental stage Anatomical site involved
99
2 different types of lineage in haematological malignancy
Myeloid or lymphoid
100
Naming haematological malignancies based on developmental stage
Blastic is primitive Cytic is more mature
101
What is the exception to naming haematological malignancies based in anatomical site involved
Chronic lymphocytic leukaemia Can involve both blood and lymph nodes
102
Features of histological aggression in haematological malignancies
Large cells with high nuclear-cytoplasmic ratio Prominent nucleoli Rapid proliferation
103
Features of clinical aggression in haematological malignancies
Rapid progression of symptoms
104
What are immunoglobulins
Antibodies produced by b cells and plasma cells
105
What are immunoglobulins made from
Proteins made from 2 heavy chains and 2 light chains
106
What determines the class of antibody produced
The heavy chain type
107
How can immunoglobulins be used
Can be expressed on B cell surfaces Released into the blood stream as antibodies by plasma cells
108
Role of B cells
Antibody production Act as antigen presenting cells
109
Role of plasma cells
Produce large quantities of antibody
110
Polyclonal increase in immunoglobulins
Ig produced by many different plasma cell clones
111
What does polyclonal increase in immunoglobulins indicate
A reactive cause
112
Monoclonal increase in immunoglobulins
All derived from clonal expansion of a single B cell
113
What are the 2 ways we can detect immunoglobulins
Serum electrophoresis Serum immunofixation
114
Bence jones protein
Immunoglobulins light chains present in myeloma
115
How do we detect Bence jones protein
Urine electrophoresis and immunofixation