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Bio 107 > Blood circulation > Flashcards

Blood circulation Flashcards

1
Q

Systolic Pressure

A

LV at full contraction

Bp normal 120 (systolic) / 80 (diastolic)

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2
Q

Major components of blood

A 
Proteins
Vitamins, Hormones
Cells 
Lipids
Electrolytes
Glucose
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3
Q

At what Partial Pressure of oxygen and to what does it freely bind to, partial pressure dissociation

A

@ 100 mm Hg
O2 binds freely to Fe2+

As p(O2) decreases, O2 dissociates and is replaced by CO2

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4
Q

What does cyanide target and what does its effect on haemoglobin?

A

Forms cyanohaemoglobin (pink)

Targets Fe2+ containing cytochrome C oxidase (mitochondria), essential for respiration

Stops heart mucsles

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5
Q

What is the pH of blood and what is it buffered by?

A

7.4

Albumin, bicarbonate (HCO3-), creatinine, phosphate
ABCP

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6
Q

What is Hematocrit?

A

RBC : Total blood volume

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7
Q

Layers of blood by centrifugation, and its %

A

Plasma (50%) - viscous/thick, uncoagulated blood, serum normally yellow after fatty meal due to lipids

Buffy Coat (10%) - WBC’s, platelets

RBC’s (40%)

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8
Q

Why is fibrinogen absent in serum?

A

As it has formed an insoluble fibrin clot

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9
Q

Erythrocytes quantity, function and structure

A

RBC’s
5/6 million per mL
Carries oxygen, biconcave, no nucleus

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10
Q

Leukocytes quantity, function and structure

A

WBC’s
10,000 per mL
Immune defence

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11
Q

Platelets quantity, function and structure and where it is derived

A

400,000 per mL
Coagulation and tissue repair
Bi-concave, no nucleus

Derived from megakaryocytes

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12
Q

What are the 5 major proteins in blood separated by electrophoresis?

A 
Albumin
a1
a2
B
Y (gamma)
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13
Q

Plasma

A

Viscous/thick liquid fraction without cells

Contains fibrinogen removed before electrophoresis by coagulation

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14
Q

Serum

A

Less viscous yellow liquid AFTER removal of clot (fibrinogen)

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15
Q

What are the 2 groups separated by serum electrophoresis?

A

Albumin (50%)

Globulin (40%) - a1, a2, B, Y

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16
Q

What is and how is Multiple Myeloma diagnosed?

A

Form of leukaemia, malignant mature B-lymphocyte produces antibody (monoclonal Ig) in v high amounts.

By serum electrophoresis, as it shows large peak of Ig

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17
Q

What is the most abundant protein in blood and what is its function?

A

Albumin- 50% of total blood protein

Maintains/provides osmotic pressure

“SPONGE”- absorbs fluid- balance

Binds and transports small molecules, proteins, hormones

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18
Q

What is fibrinogen cleaved by and how is it activated

A

Cleaved by Thrombin- forming cross-link fibrin

By coagulation cascade

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19
Q

Function of Immunoglobins (Ig) / Antibody, where are the produced

A

10% of total blood
Immunity- elevated in disease
Produced by plasma B-lymphocytes

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20
Q

Complement (C’) proteins function, most abundant component

A

9 major components ‘coat’ bacteria for phagocytosis- opsinization- signal neutrophils

Zymogens (inactive till cleaved)- most abundant is C3

Innate immunity

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21
Q

Coagulation proteins, what ion is required for blood clotting

A

13 proteins contribute
Enzyme Thrombin cleaves fibrinogen
Ca2+ required for clotting

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22
Q

What is haemophilia and its most common form?

A

X-linked recessive

Factor VIII deficiency

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23
Q

Electrolytes Functions

A

Ca2+ and K+ - help with blood clotting

Isotonicity (two solutions of same conc. of solutes)

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24
Q

Origin of blood and original cell

A

Bone marrow

Pluripotent (can give rise to several different cell types)

Haemotopoeitic stem cell (CD34+)

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25
Q

CD34+ gives rise to, and is most abundant in

A

Myeloid (partly form innate immunity) and lymphoid (adaptive immunity)

Umbilical cord blood

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26
Q

What cell gives rise to all innate immunity cells

A

Myeloblast

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27
Q

What are the three factors that drive haemotopoiesis

A

GM-CSF
G-CSF
EPO

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28
Q

Where is GM-CSF produced? What does GM-CSF stimulate production of

A

produced by TEF:
T-lymphocytes
Endocrine cells
Fibroblasts

stimulates production of: INNATE Immunity (BENM)
Basophils
Eosinophils
Neutrophils
Monocytes
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29
Q

Where is EPO produced? What does EPO stimulate production of

A

Produced in Kidney and Liver

Stimulates production of RBC’s

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30
Q

What does G-CSF stimulate production of, what does it mature?

A

Stimulates production of:
Granulocytes (eosinophils, basophils), stem cells

And it matures neutrophil

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31
Q

Stem cells

A

When it divides, new cell can either remain a stem cell or become another type of cell with a more specialized function
E.g. bone marrow, repair damaged/worn out tissue

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32
Q

Myeloid progenitor

Phagocytosis and Innate Immunity

A 
Gives rise to: EMMM
Erythrocytes
Myeloblasts (--> BENM)
Megakaryocyte (--> thrombocytes) 
Mast cells

EMMM (every man makes money)

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33
Q

Lymphoid Progenitor

A

B (plasma cell) and T (Immature T’s give CD4, CD8) lymphocytes

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34
Q

Three pathways of activating Complement

A

Classical
Alternative
Lectin

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35
Q

Classical Activation

A

Antibodies (IgM or IgG) bind to microbe surface

C1,2,3,4 condense on antibody –> (C2aC4b) = C3 convertase on surface

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36
Q

Alternative Activation

A

C3 activated by being close to surface of microbe
This activated another type of C3 convertase

C3 protein cleaved by C3 convertase –> C3b + C3 –> C5 convertase

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37
Q

Lectin Activation

A

Doesn’t recognise an antibody bound to its target

Lectins are carbohydrate binding proteins in blood that bind to unusual carbohydrates found only on microbes

Complement condenses on these bound lectins

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38
Q

End stage complement

A

Surface bound convertases activate complement 5-9 forming lytic pore (MAC) causing bacteria to lyse

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39
Q

Anaphylotoxins

A

C3a,C4a,C5a (chemoattractants) recruit and activate phagocytes to site of infection

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40
Q

Virulence factors

A

Proteins produced by microbes that inhibit complement cascade

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41
Q

Phagocytic cells

A

Neutrophils and macrophages have complement receptor that bind complement and initiate phagocytosis

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42
Q

2 Coagulation pathway’s and result

A 
Intrinsic pathway (contact)
Extrinsic pathway (tissue damage)

Results in binding and activation of platelets that bind to vessel cell wall

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43
Q

Intrinsic pathway

A

Factors 8, 9, 11, 12

Leads to cleavage of Factor X- converts prothrombin -> thrombin

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44
Q

Extrinsic

A

Factors 5, 7

Activate Factor X

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45
Q

Thrombin use

A

Cleaves fibrinogen -> fibrin

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46
Q

Fibrin

A

Forms cross-links forming clot

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47
Q

Anti-coagulants

A

Produced by Hirudin, Heparin, Warafin, Mosquitoes

Block thrombin, preventing clotting

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48
Q

What dissolves clot in blood

A

Plasminogen-> Plasmin
Plasminogen - activated by Tissue Plasminogen Activator (TPA) or streptokinase

Plasmin cleaves fibrin clot

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49
Q

Thromolysis

A

Plasmin cleaving fibrin clot

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50
Q

What does TPA and streptokinase prevent

A 
Myocardial infarct (heart attack)
Pulmonary embolism (clot in lungs)
DVT (clot usually in leg)
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51
Q

Innate immunity features

A

Doesn’t change/strengthen over time

No memory (1st and 30th response the same)

Immediate/rapid response

Recognises broad range of pathogens using small set of receptors

Distinguish self from non-self

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52
Q

Cellular Response and examples

A

Myeloid, Lymphoid cells
Phagocytosis, cytotoxic T-cells
Release of cytokines

Examples:
BENM + dendritic cells, natural killer cells

53
Q

Humoral Response and examples

A

Soluble factors that can directly kill bacteria

Examples
Antimicrobial peptides
Antibodies produced by B-cells
C-reactive protein
Complement
LPS binding protein
Mannose binding lectin
54
Q

3 types of innate immunity processes

A

Complement
Phagocytosis
Pattern recognition receptors (PRR)

55
Q

Innate immunity complement process

A

Opsonisation of microbes by blood proteins and production of anaphylotoxins (chemoattractant) that attract & activate phagocytes

56
Q

Innate immunity phagocytosis process

A

Engulfing by neutrophils or macrophages destroying organism

57
Q

Innate immunity Pattern recognition receptors (PRR)

A

Recognise complex microbial molecular patterns

Found on many myeloid cells

58
Q

Viruses function, examples

A

Intracellular pathogen, use host machinery for replication

Examples
Influenza, smallpox, HIV, Polio, varicella (chicken pox)

59
Q

How is bacteria distinguished, destroyed and give examples of bacteria

A

Mostly extracellular, engulfed by phagocytic cells
Most distinguishable by gram stain

Examples
Staph aureus - (boils, skin peeling)
Strep pyogenes - (swollen throat, lymph nodes)
Mycobacterium Tb - (cough, fever)
Vibrio Cholera
Yersinia pestis (plague)
60
Q

How are Protozoa and parasites destroyed? What are Protozoa and parasites

A

Complex, mostly multicellular organisms

Direct killing by cytotoxic chemicals released by myeloid cells
CANT BE ENGULFED so BEM secrete chemical mediators (histamine)

Examples
Malaria
Helminths ‘worms’

61
Q

Gram positive and examples that show +ve

A

Thick peptidoglycan cell wall as defence
Phagocytosis needed, not directly killed by complement

Examples
Staph aureus
Strep pyogene

62
Q

Gram negative and examples that show -ve

A

THIN peptidoglycan layer
Killed by complement MAC lysis, directly killed

antibiotics (e.g. penecillin) block peptidoglycan synthesis, bacteria can’t divide

Examples
E-coli
H. Influenza

63
Q

1st step in recruiting a neutrophil (extravasation)

A

Activation

Chemokines from site of infection activate endothelial cells to express adhesion molecules

Neutrophils express adhesion counter receptors

64
Q

2nd step in recruiting a neutrophil (extravasation)

A

Tethering

Neutrophils slow down and tether (roll) along endothelial cells inside capillary

Slalyl Lweis X (carb) on neutrophil forms bonds in selectins on endothelial cells

65
Q

3rd step in recruiting a neutrophil (extravasation)

A

Adhesion

Strong binding between neutrophil integrins and ICAM-1 on endothelial cells stops neutrophil from rolling

Neutrophil changes shape, flattens out

66
Q

4th step in recruiting a neutrophil

A

Diapadesis

Neutrophil squeezes between endothelial cells into interstitial space (capillary –> tissue)

67
Q

5th step in recruiting a neutrophil

A

Chemotaxis

Neutrophil travels to site of infection guided and travelling down chemokine gradient

68
Q

Phagocytosis of opsinised cells

A

Bacteria treated with serum to opsonise them
Neutrophils detect c5a (chemoattractant) by their receptors on leading edge

Neutrophils migrate up chemoattractant gradient

  • Polymerising actin @ leading edge
  • De-polymerising actin @ trailing edge

Phagocytes mainly bind to C3b via receptors on microbe surface

69
Q

Which complement receptor is the most important? what does this receptor bind to

A

C1 (MOST IMPORTANT) binds to C3b

70
Q

Fc Receptor mediated phagocytosis

A

Ingestion- bacterium engulfed by Fc receptors on neutrophils binding to Fc on antibody

Fusion- Phagosome + lysosome -> phagolysosomes

Acidification- Phagolysosome acidifies with H+ pumped in

Digestion- Proteases activated from acidification, stimulating production of superoxides (H2O2 and HOCl)

Exocytosis- removal of digested microbe

71
Q

Pattern Recognition receptors (PRR)

A

PRR recognise pathogen associated molecular patterns (PAMPS) - unique to microbes

Best known PRR’s are Toll-like Receptors (TLR)- Leucine rich repeat (LRR)

Activation of TLR activates strong inflammatory response

72
Q

Pattern associated molecular patterns (PAMPS) and example

A

LPS- lipopolysaccharides
Evolutionarily stable
‘power switch’ for adaptive response

73
Q

LPS- lipopolysaccharides

A

Tiny amounts induce powerful response
Gram negative bacteria

Pyrogen

  • causes fever, rigors (shivering), hypotension (low BP)
  • this condition known as SEPTIC SHOCK- due to uncontrolled gram negative infection in blood
74
Q

Which bacteria are gram +ve, -ve or neither

A 
Staph aureus (+ve)
Strep. pyogenes (+ve)

Mycobacterium tuberculosis
(NEITHER- due to think LIPID cell wall)

Yersinia Pestis (-ve)
Vibrio Chlorae (-ve)
75
Q

Adaptive Immunity

A

Memory (each successive response is stronger, more effective)

Affinity of B-cells towards antigen increases with time and perspective of antigen

Born with large repertoire of B&T lymphocytes

76
Q

How is the large repertoire of B&T lymphocytes produced

A

Randomly produced by gene rearrangement that codes for antigen receptors

77
Q

Where are B&T lymphocytes produced

A

Bone marrow, thymus, spleen

78
Q

What is the specificity of each lymphocyte?

A

Different specificity on each antigen

ONE B cell = ONE antigen specificity

79
Q

Transposon

A

“jumping gene”
DNA sequence that can move to new positions within genome
It is inserted into receptor gene

80
Q

Transposase

A

Enzyme bound to end of transposon allowing it to move to other parts of the genome,

‘in trans’- Rearrange other genes without affecting its own receptors

81
Q

What is tranposase now called?

A

RAG 1 & 2 (recombination activation gene)

82
Q

What are Recognition sequences (RS) and how are they shifted out

A

base pair sequences found @ ends of any gene segments that rearrange

Shifted out by RAG 1&2, to be recombined with other sequences

83
Q

Immunoglobin fold, approx. how many amino acids

A

two anti-parallel B-sheets

30 degree twist to each other, forms soluble “B-barrel structure” (approx. 110 a.a’s)

84
Q

What makes up immunoglobulin domains?

A

7 (constant) or 9 (variable) B-strands

85
Q

How are the B-sheets stabilised?

A

Single disulphide bond between sheets

86
Q

How are B-strands connected? and what do the “connections” do?

A

Loops

Loops are not constrained, extreme amino acid diversity

87
Q

Ig Antibody structure

A

4 protein chains, 2 heavy chains, 2 light chains

4 loops on Heavy chain, 2 on light chain

88
Q

What are the two parts of a H and L chain

A

Variable and Constant region

Variable region is where loops of a.a. diversity occurs

89
Q

How many loops per variable region on each chain

A

3 per variable region per chain, 6 in total per antigen binding site region

90
Q

Effector region

A

Bound by Fc receptors on myeloid and complement`

91
Q

IgM properties, 2 different forms

A

Default Ig, made by ALL B-cells (naive)
Low affinity

Membrane form- B-cell antigen receptor (BCR)
Soluble form- Pentameric structure (10 antigen binding sites)

LOW affinity as its naive- doesn’t know what antigen it is going to bind to

HIGH avidity “stickiness”- good at fixing complement

Good @ binding to microbe surfaces

92
Q

Affinity, example

A

“how good @ finding each other”

Sum of attractive forces @ two surfaces exceeds repulsive forces- so bind together

Antibodies v. high affinity, less antigen required for immune response to be initiated

93
Q

Avidity, example

A

“Velcro”

Multiple affinity contact points
Individually weak, LOTS together= strong

IgM (e.g. 10 contact points, stronger than 1)

94
Q

IgG

A

MOST abundant
Activates complement
Placental transfer

95
Q

IgA

A

Secreted @ mucosal surfaces

In breast milk gives strong gut immunity for baby

96
Q

IgD

A

Membrane-form

2nd LEAST abundant

97
Q

IgE

A

LEAST abundant
Causes atopic allergy
High affinity receptor on mast cells, activated when IgE binds to e.g. pollen and allergens

98
Q

Why can a.a’s form complementarity to most things?

A

A.a diversity @ antigen binding site is huge

99
Q

Where is the a.a. variation found? and what do they do?

A

3 regions of Complementary Determining Regions (CDR)

These are the 3 loops that connect the strands in the 1st domains of the H and L chains

6 in total- connect B-strands in the Ig variable domain ( first N terminal domain in H chains and L chains

100
Q

How many loops in an antigen binding sites? Area of surface

A

3 loops from VH and 3 from VL juxtapose in the folded protein

Roughly rectangular surface of ~800-1000 Å^2

Two ABS per antibody

101
Q

Recombination

A

1 D segment combines with 1 J segment
everything in between is lost, (e.g. introns)

RAG 1 & 2 bring these two segments from long distances together

double strand unwinds, editing; adding and deleting bp’s occur before strand is rewound

102
Q

2 step of recombination

A

1 V segment joins with 1 D segment, producing VDJ segment

Huge variation in VDJ segments

VDJ codes for CDR3, center

103
Q

Somatic hypermutation

A

One Naive B-cells has the IgM receptor for the antigen for the antigen

Then replicates to form progeny which undergo random mutation of gene adding to the VDJ gene

104
Q

Where does clonal selection occur in body

A

In B-cell follicles in your lymph nodes

105
Q

How does a cell achieve a higher affinity receptor?

A

Successive rounds of affinity maturation, B-cell is mature

106
Q

What can mature B-cell become?

A

Plasma cell- secretes high affinity soluble IgG

Memory cell- resides in lymph nodes long-term waiting for next encounter with that antgen

107
Q

How does immune system produce antigen receptors to encounter all antigens in the future?

A

Stochastic gene rearrangement

Produces as many possible antigen receptor combinations as it can

108
Q

Fundamentals behind vaccination

A

Weak naive B-cell undergoes rearrangement & hypermutation eventually secreting high affinity IgG

Next time you are exposed to antigen, high affinity IgG neutralises pathogen before it can grow/damage

109
Q

What is the molecular weight of IgG?

A

150 kDA (kilodaltons)

110
Q

Molecular weight of Heavy and Light chain?

A 
HC = 50-75 kDa 
LC = 25 kDa
111
Q

Thymus

A

Where immature lymphocytes from bone marrow mature

Gland sits above heart, largest at birth, decreases with age

112
Q

What surface antigens are expressed on T-lymphocytes

A

MHC class 2- CD4
80% of T-cells
secrete cytokines –> drive immune response

MHC class 1- CD8
20% of T-cells
Cytotoxic cells, kill other infected cells
Suppress autoimmune cells

113
Q

Derivatives of CD4

A

T-reg (suppress immune system)
Th-1 (cellular immunity/response)
Th-2 (antibody immunity/ humoural response)
Th-17 (promotes inflammation)

114
Q

How is T-cell signalling initiated by CD4 and CD8

A

CD4 and CD8 contain tyrosine kinases (transfer phosphate group from ATP to protein); causing phosphorylation

115
Q

T-cell receptor (TcR)

A

Ig like molecule on ALL surfaces on T-lymphocytes
TcR gene locus undergoes rearrangement like in B-cells

Two gene loci- a-chain and B-chain

Only recognise ONE antigen (unlike antibodies)

116
Q

Major Histocompatibility Complex (MHC)

A

“flags”

present virus or bacteria to surface of cells to T-cells

117
Q

T-cells see what two antigens @ the same time

A

Foreign peptide antigen (non-self) imbedded in MHC - encoded by virus

MHC molecules (self)

118
Q

Cytotoxic T-lymphocytes (CTL)

A

Can only kill infected cells from own strain (congenic mouse experiment)

Restricted by MHC, as only difference between epithelial cell C and D was in the MHC cells (present antigens differently)

119
Q

Polymorphic

A

More than one form, varies between individuals

Each polymorphic gene as 12 copies

120
Q

MHC restriction, structure

A

TcR is membrane bound like Ig molecule on T-cells
6 loops, CDR 1,2,3 each have 2- variable region many combinations

antigen binding surface of TcR binds to top of MHC “peptide groove” (contains foreign peptide antigen)

MHC molecules expressed on most cells and present antigens to T-cells. HIGHLY POLYMORPHIC`

121
Q

Two different classes of MHC, and HLA parts

A

HLA- human leukocyte antigens

Class 1 = HLA A, B, C
Class 2 = DP, DR, DQ

Each gene has 2 alleles, 12 in total
2 Parental alleles are CO-DOMINANT

122
Q

MHC class 1

A

Picks up peptide antigens from inside the cell

Presents them to CD8 cytotoxic T cells

123
Q

MHC class 2

A

Picks up digested antigens from phagolysosome (extracellular pathogens) and present them to CD4 helper cell

124
Q

CD4 helper T-cells

A

Phagocytic cell takes up bacteria, some captured by MHC class 2, expresses it on surface, where it is recognised by CD4 helper cell

MORE helper T-cells produced which produce cytokines that “help” other cells replicate

125
Q

What destroys CD4+

A

HIV. Uses CD4 antigen as its receptor to enter and replicate in helper T-cells

126
Q

AIDS

A

Resulting from long-term depletion in CD4 T-cells

Lose ability to respond to simple infections

127
Q

Why is no vaccine available for AIDS

A

Have 100’s of viral mutants that can’t all be covered by vaccine

128
Q

Problem with transplantation

A

T-cells of recipient recognise MHC donor antigens as foreign

129
Q

What suppresses T-cell response in transplantation recipients

A

Immunosuppresive drug (cyclosporine)

Bio 107 (4 decks)

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