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BIOSCI 107 (modules 4-7) > 5.1 blood and immune - pts 1-3 > Flashcards

5.1 blood and immune - pts 1-3 Flashcards

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1
Q

what are three uses of serology

A
  1. detect historial infection
  2. estimate prevalence in a population
  3. understand protection and persistence
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2
Q

how is prevalence of pathogens in population determined

A

serosurvey of antibodies within a population

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3
Q

what is S spike protein

A

the surface antigen on SARS CoV 2

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4
Q

what are three ways pathogens can enter the body

A
  1. eating
  2. breathing
  3. skin wounds
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5
Q

what are anatomical barriers of the innate immune system

A
  1. skin - a physical barrier, and pores contain antimicrobial fluid e.g sebum and sweat
  2. secretions, e.g stomach acid, mucus, enzymes
  3. mucous membranes, e.g gut and respiratory tracts
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6
Q

what was the cause of the post-covid respiratory illness surge

A

a drop in antibodies due to lower exposure to pathogens during lockdowns

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7
Q

what is immunogenicity

A

the ability to trigger an immune response leading to production of antibodies and immune cells

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8
Q

bacteria multiples _____ (i.e speed)

A

rapidly, can double in 20 mins

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9
Q

relationship between B-cell receptor and antibodies

A

B-cell receptors are two armed receptors for epitopes, which upon activation release soluble versions of themselves which recognise the same epitopes, which are antibodies

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10
Q

what is hypertension and what does it cause?

A

too high blood pressure, can cause capillaries rupturing, stroke, and blood clotting

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11
Q

large vessels near heart have high blood____ and low _____

A

high volume, low flow

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12
Q

small capillaries far from heart have high blood ____ and low _____

A

high flow and low volume

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13
Q

role of the pulmonary artery

A

takes oxygenated blood from right side of heart to lungs

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14
Q

why do arteries squirt blood

A

because they have thick muscular walls creating constant pressure to keep blood moving

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15
Q

veins structure and function

A

have thinner walls and low pressure, have valves to prevent back flow. transport deoxygenated blood back to the heart.

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16
Q

colour of oxygenated vs deoxygenated blood

A

oxygenated is bright red, while deoxygenated is dark red

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17
Q

what important ventricle has thick muscular walls

A

the left ventricle, as it pumps oxygenated blood to the the whole body

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18
Q

what is atopic allergy

A

allergic response to common environmental triggers, leading to immune overreaction mediated by excess IgE

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19
Q

what is hypotension and its risks?

A

low blood pressure.
faintness, dizziness, fatigue.

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20
Q

describe the structure of alveoli

A

small air sacs with a capillary network, made of endothelium (one-cell thick)

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21
Q

pO2 is higher/lower in the lungs than tissue?

A

higher

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22
Q

structure of haemoglobin and how this enables it to do gas transport

A

4 haem molecules, containing 1 Fe2+ each which can pick up things with lose electrons (oxygen)

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23
Q

Fe2+ picks up lots of things more readily than oxygen; name 2, the colour they would manifest as in blood, which is more deadly, and their poisonous mechanism

A

cyanide; cherry red in blood, more deadly, binds to C IV in the ETC.
carbon monoxide; pinkish in colour, less deadly, binds to Fe2+ in haemoglobin, preventing oxygen binding.

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24
Q

pCO2 is higher/lower in the lungs than tissue?

A

lower

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25
5 main blood proteins
albumin, haemoglobin, immunoglobulins, fibrinogen/coagulation proteins, complement proteins
26
role of albumin
provides bulk and acts as a buffer to prevent blood pH and osmolarity changes, binds many small molecules
27
why is the 'buffy coat'
layer of white blood cells and platelets between the plasma and red blood cells in centrifuged blood
28
what does Carboxyhaemaglobin carry
carbon monoxide
29
what does carbamihaemoglobin carry
carbon dioxide
30
normal pH of blood, and some compounds that effectively buffer this
7.4, albumin, phosphate, bicarbonate
31
how to recognise monocytes, lymphocytes, neutrophils, and other granulated leukocytes
monocytes are larger with horse-shoe nucleus, lymphocytes are small and round, neutrophils have segmented nuclei, other granulated leukocytes have granules
32
what cells are useful after chemotherapy for leukaemia patents, and how
CD34+ stem cells, by being removed before chemo then reintroduced after with stimulating factors GM-CSF and G-CSF
33
AIDS is identifiable by:
CD4+ deficiency
34
what are MACS and FACS and how do they work
MACS - magnetic-activated cell sorting, labels antibodies with magnetic beads FACS - fluorescence-activated cell sorting, uses lasers and fluorescent proteins or dyes
35
complement/complement proteins are:
a set of 9 plasma proteins that regulate opsonisation and phagocytosis
36
what are convertases, what is their function
enzyme complexes formed from groups of complement proteins, activate more complement/ amplify the response
37
what are lectins and the lectin pathway to complement activation
lectins are carbohydrate binding proteins that bind to carbohydrate molecules distinct to microbes, activating similar convertase to classical pathway
38
what makes up most of a RBC's weight
haemoglobin
39
what is the colour of serum and what is/isn't in it
straw yellow, can be cream coloured after fatty meals due to lipids. fibrinogen absent, as coagulation has occurred.
40
what is the colour of plasma and what is/isn't in it
yellowish, contains fibrinogen and anticoagulants (to avoid clotting and transforming to serum)
41
what produces immunoglobulins
plasma cells, made from B cells
42
why do erythrocytes not get as damaged (as leukocytes) after radiotherapy
as they have no nucleus, so no DNA to be altered
43
how, and what to, are convertases bound?
microbial surfaces, irreversibly by covalent bonds
44
how does classical pathway of complement activation work
IgM or IgG binds to microbe surface, activating C1 and a proteolytic cascade resulting in C3 convertase on microbe surface.
45
how does alternative complement activation pathway
uses only protein C3 when it is very close to bacteria surface, activating a C3 convertase.
46
what are anaphylotoxins, where did they come from
form during the complement cascade, are small complement fragment C3a C4a and C5a that attract other immune cells, trigger inflammation, and increase vasopermeability (leading to edema/leaked fluid)
47
how, besides from complement, can phagocytosis be triggered?
FcR mediated phagocytosis. Myeloid cells have Fc receptors, which bind to Fc region of antibodies bound to microbe surface, activating phagocytosis.
48
how do phagocytes (neutrophils) find infection?
neutrophil extravasation: 1. activation - chemokine or inflammation activates local endothelium of capillaries 2. tethering - unregulated adhesion molecules (selecting) recognise sialyl lewis X on neutrophils, and grab them, slowing them down 3. adhesion - binding between neutrophils interns and ICAM- on endothelium causes neutrophil to halt and flatten on the cell 4. diapedesis - neutrophil squeezes out of the blood vessel through the endothelial cells 5. chemotaxis - neutrophil migrates along chemoattractant gradient to find infection/bacteria
49
how does phagocytosis proceed
1. capture/ingestion of bacteria 2. phagocyte membrane invaginates to enclose bacteria in a phagosome 3. phagosome fuses with lysosome to form phagolysosome 4. phagolysosome kills bacteria by acidifying by pumping in H+ and producing superoxides 5. exocytosis to expel digested microbe
50
describe viruses
intracellular pathogens which can only reproduce inside cells, simplest form of life with essentially only RNA surrounded by a capsule.
51
what are the three types of pathogens and what processes counteract them
viruses - antibodies and cellular immunity bacteria, yeast, fungi - phagocytosis complex organisms like protozoa and parasites - destroyed by chemicals from granules (too big for phagocytosis)
52
what does penicillin do to bacteria
inhibit formation of the peptidoglycan carbohydrate wall
53
gram negative vs positive bacteria: structure and effective immune response
gram positive: thick peptidoglycan wall, resistant to MAC so must be phagocytosed. gram negative: thin peptidoglycan wall and tough outer membrane. more sensitive to MAC lysis.
54
end phase of complement
process beginning from activation of C5, which along with other complement proteins forms a lytic pore called MAC (membrane attack complex) in bacteria, causing it to lyse/burst.
55
what are opsonins
molecules formed from complement that coat bacteria to flag them to phagocytes
56
most abundant complement protein in blood?
C3
57
what are virulence factors
molecules produced by pathogens to inhibit the immune system response
58
describe activation/first stages of intrinsic coagulation pathway
occurs when blood contacts a foreign surface like glass or metal prosthetics, involves a range of factors which converge on factor X.
59
describe activation/first stages of extrinsic coagulation pathway
occurs when blood encounters tissue factor (TF) due to tissue damage, e.g bruises and cuts. involves a range of factors which converge on factor X.
60
what is/role of factor X
inactive protease enzyme that becomes factor Xa (activated) which cleaves prothrombin to thrombin.
61
name anticoagulants and anticoagulant producers, and how they work
hirudin produced by leeches, heparin, mosquitoes. bind to thrombin and inhibit it from cleaving fibrinogen.
62
how is fibrin clot formed and dissolved?
fibrinogen is cleaved by thrombin, forming fibrin, which crosslinks to form a clot. plasminogen is cleaved to plasmin, which is an enzyme that dissolves clots.
63
what is haemophilia, and its most famous/common type
type of genetic disorder resulting in defective coagulation factors. most famous type was carried by queen victoria, X-linked recessive trait resulting in deficiency in factor VIII.
64
thrombolytic drugs names and functions
TPA and streptokinase. used to treat thrombus-related diseases like stroke, pulmonary embolism, myocardial infarct.
65
important non-coagulation-factor molecule for coagulation
calcium
66
viruses are mainly ____ while bacteria are mainly ____, and parasites/protoza are ______
intracellular, extracellular, multicellular and extracellular
67
PAMPs are
pathogen associated molecular patterns: evolutionary stable molecular structures on pathogens
68
PRRs are
pattern recognition receptors, which are cell protein receptors for PAMPs which signal the immune system to respond
69
structure and function of most known PRR
toll-like receptor. has lots of leucine repeating (LRR) coils, making it look like a slinky. bind complex PAMPs and signal powerful inflammatory response involving nuclear factor NFkB.
70
what is LPS, what are its consequences, and how is it bound
lipopolysaccharide, a PAMP on all gram-negative bacteria. it is pyrogenic, and can trigger sepsis. bound (at lipid A portion) by TLR4 and serum/lipid-binding protein MD2
71
what is sepsis and septic shock
sepsis occurs when body's response to an infection damages its own tissues and organs. septic shock is a consequence of this, where hypotension leads to extreme blood pressure drop.
72
neutrophils recognise C3/C3b by what?
CR1 (complement receptor 1)

BIOSCI 107 (modules 4-7) (4 decks)

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