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Sandra phase 1 > Blood > Flashcards

Blood Flashcards

1
Q

Too little RBC in blood?

A

Anaemia <45%

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2
Q

Too much RBC in blood?

A

Polycythaemia >45%

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3
Q

Too little WBC in blood?

A

Leukopenia <4,800ul

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4
Q

Too much WBC in blood?

A

Leucocytosis >11,000 ul

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5
Q

Too little platelets in blood?

A

Thrombocytopenia <150,000ul

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6
Q

Too much platelets in blood?

A

Thrombocytosis >450,000 ul

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7
Q

Plasma composition

A

H20- 90-93%
Plasma protein-8%

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8
Q

Plasma protein composition

A

Albumin (60%)
Globulins (40%)

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9
Q

Iron deficiency symptoms?

A

Shortness of breath
Fatigue
Tachycardia
Dizziness

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10
Q

What do we need iron for?

A

Iron reacts with protoporphyrin (pigment in RBC) converts it to haem. Haem is essential for haemoglobin. Therefore less iron-less haem-less haemoglobin

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11
Q

What happens if there is less haemoglobin in the blood due to iron. Related condition

A 
Iron deficiency (condition)
It takes up most volume in blood and therefore becomes Microcytic- decrease in MCV less than 80fl.
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12
Q

Causes of Fe2+ deficiency

A

Blood loss
Heavy menstruation
Low iron diet

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13
Q

B-12/Folic Acid/(Pernicious anaemia) how does it take place?

A

Main cause is autoimmune
Reason: Parietal cells in stomach have glycoprotein called intrinsic factor. B12 naturally bind to intrinsic factor. However in pernicious anaemia antibodies are produced which bind to the intrinsic factor blocking B12.
Less B12 in bloodstream
Result in macrocytosis (MCV <90fl). Can get stuck

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14
Q

What is B12 needed for?

A

Needed in order for red blood cells DNA to mature, synthesis and condense

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15
Q

What is folic acid needed for?

A

DNA maturation

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16
Q

Treatment of pernicious anaemia?

A

Intra muscular injections of B12

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17
Q

What is hereditary spherocytosis

A 
Genetic
Mutation (ankyrin and spectrin) results in a spherical haemoglobin-loses its biconcave shape. Not good at delivering oxygen effectively as it gets stuck
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18
Q

Hereditary spherocytosis symptoms

A

Splenomegaly
Haemolysis

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19
Q

How to detect hereditary spherocytosis?

A

Coombs test

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20
Q

What is sickle cell anaemia (HbS)

A

Missense mutation

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21
Q

When in sickle cell anaemia does haemoglobin have its sickle shape?

A

When its not bound to oxygen

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22
Q

What can sickle cell anaemia lead to?

A

Vaso-occlusive crisis

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23
Q

Treatment of sickle cell anaemia

A

oxygen
pain reliever
fluids

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24
Q

Sickle cell anaemia can mean that your immune to what?

A

Malaria

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25
Q

Types of anaemia

A

Fe2+ defiecncy
Aplastic
Haemorrhagic
B12/Folic
Thalassemia
Sickle cell
Hereditary spherocytosis

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26
Q

Where is thalassemia more common in?

A

Mediterranean ancestry

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27
Q

What is thalassemia?

A 
Genetic condition
Two types (alpha and beta)

Missing a globin chain:

alpha: 1aplha + 2beta
beta: 2alpha + 1beta

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28
Q

Thalassemia-microcytic or macrocytic?

A

microcytic

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29
Q

Treatment of thalassemia

A

Bone stem cell transplant
Iron
Transfusion

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30
Q

Blood transfusion-

A

negative- negative & positive
positive- positive

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31
Q

What makes your blood group positive or negative

A

Rh antigen.
If you have it, your are positive of that blood group, if absent then negative.

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32
Q

Describe Rhesus disease

A

Increases chance with every birth.
Mother RH-
Baby RH+

Mother has anti D antibodies meaning that immune response will kick in and and begin to produce antibodies. Antibodies cross placenta and attacks the babies red blood cells-undergoes haemolysis can lead to haemolytic anaemia. Develop condition haemolytic disease of new-born

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33
Q

What are the two phases of blood, what is in each phase and what percentages are involved?

A

Cellular: 45% (99% RBCs, then white blood cells and platelets make up the rest)
Fluid: 55% (plasma)

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34
Q

How many litres of blood is normal for a human?

A

5 litres

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35
Q

What is haematocrit and what is a normal value?

A

the volume of red blood cells i.e haemoglobin in the blood, normal haematocrit is 0.45

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36
Q

What is haemopoiesis? In adults where does this take place?

A

the process of the production of blood cells and platelets which continues throughout life, in adults this is confined to the bone marrow

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37
Q

What is the lifetime of RBCs?

A

120 days

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38
Q

What is the lifetime of white blood cells?

A

6 hours

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39
Q

What is the lifetime of platelets?

A

7-10 days

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40
Q

Where are the precursor cells for red blood cells found?

A

The precursor cells of red blood cells are located in the bone marrow:

  • In adults this is in the axial skeleton - skull, ribs, spine, pelvis and long bones
  • In children this is in all bones
  • In utero this is in the yolk sac, then liver and spleen
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41
Q

What is precursor cells in the blood an indication of?

A

Leukaemia

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42
Q

What do hormonal growth factors do? and what is the specific type for each type of blood cell

A

Hormonal growth factors stimulate precursor stem cells to proliferate and differentiate:

  • Epo/ Erythropoietin (hormone made in kidney) = red blood cells
  • G-CSF (granulocyte colony stimulating factor) = white cells
  • Tpo = platelets
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43
Q

What happens to the oxygen dissociation curve when the pH is decreased or the temperature increases?

A

It will shift to the right

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44
Q

What happens to the oxygen dissociaton curve when the pH is increased or the temperature decreases?

A

It will shift to the left

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45
Q

Why do red blood cells have such a short lifespan?

A

Simple cells, with no nucleus or mitochondria thus cannot repair itself - why they have such a short lifespan

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46
Q

What are young red blood cells called?

A

Reticulocytes

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47
Q

What is the role of haemoglobin and what is its structure?

A

Carries oxygen from the lungs to tissues, where it transfers oxygen to myoglobin in muscles

Haemoglobin is formed of 2 alpha and 2 beta chains and 4 haem groups - has an overall quaternary structure - due to the combination of more than two tertiary structures

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48
Q

Explain the presence of varying antigen on the surface of blood cells?

A

Some people have the gene that results in the synthesis of the A antigen on the surface of red blood cells

some have the gene that results in the synthesis of the B antigen, some have both genes and some have neither.

Those who have neither are said to have O-type erythrocytes.

Thus the possible blood types are A(more common than B), B, AB (MOST RARE) & O (MOST COMMON)

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49
Q

Which antibodies are in the plasma of a type A individual?

A

anti-B antibodies

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50
Q

What is co-dominance and why is it important in blood types? What does this produce?

A

A antigen and B antigen are both codominant. They produce AB. Type AB have neither anti-A or anti-B antibodies in their plasma, has A + B antigens on surface of red blood cells - UNIVERSAL RECIPIENT

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51
Q

What is type O?

A

Type O have both anti-A & anti-B antibodies ( has no A or B antigens) in their plasma [type O is a UNIVERSAL DONOR since don’t have A or B antigens on surface of red blood cell]. O antigen is RECESSIVE

52
Q

What would happen if a type A patient was transfused with type B blood?

A

1) the anti-B antibodies in the recipients’ blood would attack the transfused blood
2) the anti-A antibodies in the donor blood would attack the recipient’s blood HOWEVER this is usually of little consequence since the transfused antibodies become so diluted in the recipient’s plasma that they are ineffective at inducing a response
- it is the destruction of the TRANSFUSED cells by the recipient’s antibodies that produce problems

53
Q

What are the Rhesus antigens? What does Rhesus positive mean?

A

C, D, E antigens. D ANTIGEN IS MOST IMPORTANT: Rhesus positive means the D antigen is present. Rhesus negative means the D antigen is not Present

54
Q

What is anaemia?

A

reduction in haemoglobin in the blood

55
Q

What is a normal haemoglobin value?

A

12.5 - 15.5 g/dl

56
Q

What condition causes raised haemoglobin?

A

Polycythaemia (caused by smoking, lung diseases, inefficient lungs meaning less O2 is exchanged so more haemoglobin is required etc.

57
Q

What are the signs of anaemia?

A

Palor
pale mucus membranes
palmar creases (pink hands)
glossitis(sore tongue)
angular stomatitis ( cracking at corners of the mouth)
kylonychia (caused by the iron deficiency - spoon-shaped nails)

58
Q

What are the classifications of anaemia?

A

Iron deficiency
B12/folate deficiency
anaemia of chronic disorder
haemolysis
bone marrow failure/infiltration

59
Q

What is haemolysis

A

Normal or increased cell production but DECREASED LIFE SPAN < 30 DAYS, red blood cells are destroyed before their 120-day lifespan

60
Q

What are white blood cells?

A

Normal white blood cells are mature cells that circulate in the blood, they are produced from immature precursor cells in the bone marrow which are derived from stem cells. The rate of production is under hormonal control of G-CSF

61
Q

What are neutrophils? What is their lifespan and what is their role?

A
  • Most numerous white cell - lifespan is 10 hours
  • Phagocytose & kill bacteria
  • Release chemotaxins (signal more white blood cells to come to the site) and cytokines (important in inflammatory response)
  • Lack of number or function results in recurrent bacterial infections
62
Q

What are B lymphocytes?

A
  • B lymphocytes: named after Bone marrow, made in bone marrow
  • stored in secondary lymphoid organs,
  • differentiate into plasma cells
  • produce immunoglobulins when stimulated by exposure to foreign antigen
63
Q

What are T lymphocytes?

A
  • T lymphocytes: made in bone marrow - MATURE in the thymus
  • some are helper cells (CD4, help B cells in antibody generation, responsible for cellular or cell-mediated immunity), some are cytotoxic cells (CD8)
64
Q

What is acute leukaemia?

A

The proliferation of primitive precursor cells usually found in bone marrow
Proliferation WITHOUT differentiation replaces NORMAL BONE MARROW CELLS

—–resulting in:
anaemia (pallor and lethargy),
neutropenia: infections (since white cells are not being differentiated)
thrombocytopenia: excessive bleeding.

THE PRESENCE OF PRIMITIVE WHITE PRECURSOR CELLS IN THE BLOOD IS A SIGN OF acute leukaemia

65
Q

acute myeloblastic leukaemia

A

AML= Malignant proliferation of the precursor
myeloblasts (unipotent stem cells) in the bone marrow, the disease primarily affects adults - 50% survive 5 years

66
Q

acute lymphocytic leukaemia

A

ALL= Malignant proliferation of the lymphoblast
precursor cells in the bone marrow, the disease primarily affects children - 80% cured

67
Q

What is high grade lymphoma?

A

lymphocytes in lymph nodes becoming malignant, very similar to leukaemia)

Classified as Hodgkin’s disease and Non-Hodgkins lymphoma (NHL),

disease usually of the lymph nodes that spreads to the liver, spleen, bone marrow and blood

68
Q

Synthesis of which coagulation proteins is vitamin K essential for?

A

Factors 10, 9, 7, and 2 (remember 1972)

69
Q

Define Haemostasis

A

arrest of bleeding, involving the physiological processes of blood coagulation and the contraction of damaged blood vessels

70
Q

Haemostasis its importance?

A

Blood is usually fluid inside blood vessels this is because:

  • The proteins of the coagulation cascade and the platelets circulate in an inactive state
  • Proteins and platelets are only activated by tissue factor, which is present in every single-cell APART from endothelial cells thus when the endothelium is punctured etc.

Blood comes into contact with tissue factors and thus starts clotting.

71
Q

blood clots inside vessel

A

thrombosis

72
Q

blood fails to clot outside vessels

A

bleeding disorder

73
Q

What is the coagulation cascade?

A

series of proteolytic enzymes that circulate in an inactive state is activated (usually by exposure to tissue factor) in a cascade or waterfall sequence

  • in order to generate the key enzyme THROMBIN which cleaves fibrinogen creating fibrin polymerisation i.e a blood clot
74
Q

What blood cells are responsible for primary haemostasis?

A

Platelets

75
Q

What is haemophilia A?

What is its incidence, causes, symptoms, and treatment?

A

1 in 10,000 males (rare)

not enough clotting factors in blood = slow clotting time or
long PTT (prothrombin time)

Deficiency in CLOTTING FACTOR VIII (8)

Bleeding into muscles and joints

Treat with factor VIII

76
Q

What is haemophilia B? What is its incidence, causes, symptoms, and treatment?

A

1 in 50,000 males (even more rare)

Less common since the gene is smaller

Deficiency in clotting factor IX (9)

Bleeding into muscles and joints

Treat with Factor IX

77
Q

What is Von Willebrand Disease?

A

Lack of Von Willebrands Factor (VWF)

  • VWF is required for platelets to bind to damaged blood vessels, so lack of VWF =
    platelet dysfunction, hence mucocutaneous bleeding
  • Usually a mild bleeding disorder
  • Mucocutaneous bleeding: bleeding in skin & mucous membranes e.g. easy bruising, prolonged bleeding from cuts, nose bleeds (epistaxis), spontaneous gum bleeding/GI loss etc
78
Q

What are acquired bleeding disorders?

A

Recent onset, not lifelong and no family history

  • Most common cause: anti-platelet or anti-coagulation medication
  • May be generalised or localised bleeding
79
Q

vitamin K deficiency treatment

A
  • Newborns are vitamin K deficient, given it at birth
  • Treat with IV vitamin K
80
Q

What is Vitamin K needed for?

A

THE CORRECT SYNTHESIS OF COAGULATION FACTORS II, VII, XI & X (2, 7, 9 & 10) - 1972

81
Q

How is Vitamin K deficiency caused?

A

malabsorption - especially in obstructive jaundice

82
Q

How can vitamin K deficiency cause bleeding?

A

coagulation factors are still produced but they do not work

83
Q

How can drugs cause bleeding?

A
  • Aspirin affects platelet function
  • Heparin and warfarin (most widely used oral anticoagulant - works by inhibiting vitamin K) affect the coagulation cascade
  • Steroids make tissues thin and cause bruising and bleeding
84
Q

What is blood coagulation?

A

Blood coagulation or clotting is the transformation of blood into a solid gel called a clot/thrombus which consists mainly of a protein polymer called fibrin.

85
Q

What are the pathways of the coagulation cascade?

A

Intrinsic= everything necessary for it is within the blood

Extrinsic= cellular element outside the blood is needed

86
Q

Where does clotting occur?

A

locally around the platelet plug

87
Q

Function of clotting

A

its function is to support & reinforce the platelet plug and to solidify blood that remains in the wound channel

dominant haemostatic defence

88
Q

Thrombin is initially generated by which pathway?

A

Extrinsic

89
Q

What is the effect of high platelet count?

A

thrombocytosis

can lead to arterial & venous thrombosis, leading to an increased risk of heart attack + stroke

90
Q

Where are platelets made and what are their precursor cells?

A

Made in bone marrow from cells called megakaryocytes

91
Q

Why might someone with liver injury experience prolonged bleeding time?

A

Because the liver produces clotting factors.

92
Q

What is exposed if you damage the endothelium of a vessel?

A

Underlying connective tissue and collagen.

93
Q

What is the role of vWF?

A

vWF binds to collagen and platelets bind to vWF.

94
Q

What happens in platelet activation?

A

The change of shape: smooth to spiculated. This increases their surface area.

95
Q

What do activated platelets synthesise?

A

Thromboxane A2
Serotonin
ADP

96
Q

What is the function of Thromboxane A2 (TXA2)?

A

It leads to further platelet aggregation.

binds to receptors of smooth muscle causing them to contract and help with vascular spasm

97
Q

What are the platelet receptors for fibrinogen?

A

glycoprotein IIb/IIIa.

Fibrinogen forms ‘bridges’ between platelets.

98
Q

What does an undamaged endothelium release in order to prevent platelet activation in undamaged areas?

A

Prostacyclin (inhibits platelet aggregation)

NO (inhibits platelet adhesion).

99
Q

What are platelets made from? and where are they made?

A

In the bone marrow from megakaryocytes.

100
Q

In haemostasis what is prothrombin converted into?

A

Thrombin

101
Q

Give 3 functions of Thrombin.

A
  1. Converts fibrinogen into fibrin.
  2. Activates factor XIII into XIIIa.
  3. Has a positive feedback effect resulting in further thrombin production.
102
Q

What is the essential component of a blood clot?

A

Fibrin.

103
Q

Briefly describe the Fibrinolytic system.

A

Plasminogen is converted into plasmin via Tissue Plasminogen Activator.

Plasmin cuts the fibrin at various places leading to the formation of fragments.

104
Q

What is the purpose of the fibrinolytic system?

A

It acts to prevent blood clots from growing and becoming problematic.

105
Q

What is the structure of Hb?

A

2 alpha and 2 beta chains. 4 haem groups.

106
Q

What is released upon cell activation and contains a high concentration of a molecule that acts as an agonist at the platelet P2Y12 receptor?

A

Platelet dense granules.

107
Q

Give 2 reasons why the liver is important in clotting.

A
  1. The liver produces many clotting factors.
  2. The liver produces bile salts that are needed for vitamin K absorption. Vitamin K is needed for clotting factor production.
108
Q

When are the platelet receptors for fibrinogen exposed?

A

During platelet activation.

109
Q

Which of the ABO blood groups is recessive?

A

O, A and B are co-dominant.

110
Q

Why is the O blood group a universal donor?

A

It has no A or B antigens.

111
Q

What are the two ways of determining someone’s ABO blood group?

A
  1. Test using antibodies.
  2. Test for the presence of antibodies against A or B antigens.
112
Q

Describe how testing for the presence of antibodies against A or B antigens will determine someone’s blood group?

A

The presence of antibodies in the blood will indicate that this person does not have these antigens on their RBC’s. For example, if a persons blood is found to contain antibodies against the B antigen then they can’t be of the AB or B blood groups.

113
Q

Describe how testing using antibodies will determine someones blood group?

A

If the antibodies bind it indicates the presence of a specified antigen. For example, if antibodies against the B antigen bind to the patients RBC then the person must be of either the AB or B blood groups.

114
Q

What are antigens are part of the Rhesus blood group system?

A

C, D and E.

(D is the most important).

115
Q

which pathway is quicker intrinsic or extrinsic?

A

extrinsic (30 sec)
Intrinsic (4-6mins)

116
Q

How is brain involved in hypotension

A

Na+ channels in baroreceptors are closed so slower action potentials.

Slower action potentials to cardiac acceleratory and basal motor centre stimulate a sympathetic response in the medulla

117
Q

How is the brain involved in hypotension?

A

Na+ channels in baroreceptors are closed so slower action potentials.

Slower action potentials to the cardiac acceleratory and vasomotor centre stimulate a sympathetic response in the medulla

118
Q

Hearts response to Hypotension

A

Impulses from CA go to ganglions and travel to SA node and AV node release NE…
Impulses from CA go to ganglions and travel down to the myocardium-result increase in contraction

Official sympathetic fibres pass through sympathetic chain ganglions-synapse at postganglionic motor neuron cell bodies within the adrenal medulla. The adrenal medulla consists of chromaffin cells. These cells consist of postganglionic motor neurons. Release NE + Epi. Vasoconstriction + myocardium contraction

Impulses from VM go to ganglions and travel to tunica media of blood vessels. NE binds to alpha 1 adrenergic receptor and causes vasoconstriction-> decrease in diameter -> decrease in radius -> increase in TPR -> Increase in B.P

119
Q

What cells in the kidney detect blood pressure changes

A

JG cells

120
Q

What do JG cells secrete in relation to Hypotension

A

More Renin

121
Q

What causes renin to increase in kidneys in response to Hypotension

A

-Epinephrine binds to beta 1 adrenergic receptors resulting in JG cells secreting more renin is secreted as a result

122
Q

What does renin bind to and what is the result

A

Renin binds to angiotensinogen which results in angiotensin 1 being made

123
Q

How is angiotensin 1 converted to angiotensin 2

A

Takes places in lungs
angiotensin converting enzyme stimulates angiotensin 1 into angiotensin 2

124
Q

What does angiotensin 2 do?

A

Binds to zona glomerulosa receptors which secrete aldosterone

Goes to hypothalamus and stimulates anti diuretic secretion from pituitary gland

Binds to receptors on tunica media

125
Q

What causes there to be an increase of action potential to medulla due to hypertension

A

Increased stretch due to an increase in blood pressure activates the sodium channels on the sensory or afferent nerve endings of baroreceptors allowing for sodium to flow depolarizes the afferent fibres and then sends action potentials down to CN9 + CN10 into the medulla

Sandra phase 1 (16 decks)

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