Week 5 Flashcards
(139 cards)
1
Q
Define receptors. Give 4 families.
A
specialised, localised proteins whose role it is to recognise stimulants and translate this event into an activation of the cell
- enzymes
- transporters (carrier molecules)
- ion channels
- neurotransmitter, hormone or local hormone receptors
2
Q
Give the law of mass action and its applied equation to pharmacology. Define the terms.
A
the rate of a chemical reaction is proportional to the product of the concentration of the reactants
[D] + [R] [DR]
[D] = concentration of drug [R] = concentration of receptor [DR] = concentration of occupied receptors K1 rate constant for associations K2 rate constant for dissociations
3
Q
What is the equilibrium dissociation constant? Give two of its features
A
equilibrium when rate of associations = rate of dissociations
–> equilibrium dissociation constant K(D) = the concentration of drug required to occupy 50% of the receptors at equilibrium
K(D):
- different for every drug
- a measure of the affinity of any one drug for a receptor
4
Q
Which of two drugs with different K(D) values has the greatest affinity for the receptor?
A
The drug with the lowest K(D)
5
Q
Give the Hill Langmuir equation for occupancy theory, and one other way to express it
A
fractional occupancy = [D] / ( [D]+K(D) )
= [DR] / total number of receptors
= [DR] / ( [R] + [DR] )
6
Q
Give the theoretical relationship between occupancy and ligand concentration, plotted with a linear concentration scale, and plotted with a log concentration scale.
A
LINEAR CONCENTRATION SCALE
rectangular hyperbola
LOG CONCENTRATION SCALE
symmetrical sigmoid curve
7
Q
What is the pD2 of an agonist? Give the equation.
A
pD2 is the -log10 of [D] that occupies 50% of the receptors at equilibrium –> K(D)
pD2 = -log10 (K(D)) K(D) = 10^-pD2
8
Q
Which of two drugs with different pD2 values has the greatest affinity for the receptor?
A
The drug with the highest pD2
9
Q
Which blood vessels are at risk of atherosclerosis?
A
elastic arteries and medium to large muscular arteries
10
Q
Which 3 factors helped decrease death rates associated with atherosclerosis between 1963 and 2000?
A
- prevention of atherosclerosis
- improved methods of treatment
- prevention of recurrences
11
Q
Give 4 risk factors for atherosclerosis.
A
- age
- gender
- genetics
- hyperlipidaemia
- hypertension
- smoking
- diabetes mellitus
12
Q
Give 4 causes of chronic endothelial injury or dysfunction.
A
- haemodynaic disturbances
- hypercholesterolaemia
- hypertension
- smoking
- toxins
- viruses
- immune reactions
13
Q
What are the 5 effects of oxidative modification of LDL?
A
- macrophages becoming foam cells
- chemotaxis for monocytes
- inhibition of macrophages’ motility
- stimulation of release of cytokines
- cytotoxic to endothelial and smooth muscle cells
14
Q
How does a fatty streak become a mature fibro-fatty atheroma?
A
collagen and extracellular matrix deposition
15
Q
Give the morphological features of an atheromatous plaque.
A
- patchy and raised
- white to yellow
- 0.3 to 1.5cm
- core or lipids (necrotic center: cell debris, cholesterol crystals, foam cells, calcium)
- fibrous cap (smooth muscle cells, macrophages, foam cells, lymphocytes, collagen, elastin, proteoglycans, neovascularisation)
16
Q
Which 6 arteries are most likely to develop atherosclerosis?
A
- abdominal aorta
- coronary arteries
- popliteal arteries
- descending thoracic aorta
- internal carotid arteries
- vessels of the circle of Willis
17
Q
Which 5 features of atherosclerosis indicate complicated lesions?
A
- calcification
- haemorrhage
- rupture/ulceration
- thrombosis
- aneurysmal dilatation
18
Q
From when do fatty streaks develop in the aorta? in the coronary arteries?
A
aorta –> from under one year of age
coronary arteries –> from adolescence
19
Q
How many steps of atherosclerotic lesions are there? Which type can be bypassed?
A
6 steps
step 5 can be bypassed
20
Q
When do clinical features occur? What are they?
A
only occur if complications
- thrombosis
- calcification
- aneurysmal dilatation
- ischaemic events in heart, brain, lower extremities and other organs
21
Q
Give 3 measures of primary prevention and 2 measures of secondary prevention.
A
PRIMARY PREVENTION
- stop smoking
- control hypertension
- weight reduction
- lowering total LDL
- reduced calories intake
SECONDARY PREVENTION
- antiplatelt drugs in thrombosis
- lower blood lipid levels
22
Q
Make the difference between first, second and third order neurons of the somatosensory pathway.
A
FIRST ORDER
primary afferent neuron that terminates in spinal cord or brain stem
SECOND ORDER
from spinal cord/brain stem to thalamus
THIRD ORDER
from thalamus to brain
23
Q
Where is the primary (somatic) sensory cortex located?
A
in a strip posterior to the post central sulcus of the brain
24
Q
Which somatosensory area has a higher degree of localisation?
A
Area I
25
Where do the two sensory pathways partially come back together?
at the level of thalamus
26
Give the name of the 2 ascending tracts belonging to the dorsal column-medial lemniscal pathway. Indicate from where the neurons in these tracts come from
- fasciculus gracilis, from lower body extremities
| - fasciculus cuneatus, from upper body extremities
27
Which sensations does the dorsal column-medial lemniscal system carry?
discrete mechanoreceptive sensations:
- touch with a high degree of localisation
- touch with fine gradations of intensity
- phasic sensations
- movement against the skin
- position sensations from joints
- pressure sensations related to fine degree of judgment of pressure intensity
28
Which sensations does the anterolateral system carry?
- pain
- thermal sensations
- crude touch and pressure
- tickle and itch
- sexual sensations
29
Compare the nerve fibres from the dorsal column-medial lemniscal pathway to those from the anterolateral pathway.
DORSAL COLUMN - MEDIAL LEMNISCAL PATHWAY
large diameter, myelinated A-beta fibres (30-110m/s)
ANTEROLATERAL PATHWAY
smaller, myelinated A-delta and C fibres (8-40m/s)
30
Outline the path of the dorsal column - medial lemniscal pathway.
- Nerve fibres enter dorsal columns, uninterrupted to dorsal medulla
- synapse in dorsal column nuclei
- second order neurons cross immediately to opposite side of brain stem and continue up through medial lemnisci to thalamus
- medial lemniscal fibers terminate in the thalamic sensory relay area: ventrobasal complex
- third order neurons from ventrobasal complex project mainly to somatic sensory area 1
31
Which of lower extremity, face, trunk, and upper extremity is most lateral in somatic sensory area 1? which is most medial?
most lateral: face
| most medial: lower extremity
32
Where are lesions causing upper extremity ataxia located? How can the patient compensate?
lesions in cervical cord
compensation with vision
33
What does paraesthesia associated with dorsal column disease usually result from?
ectopic discharge in damaged dorsal column axons
34
Outline the the path of the anterolateral pathway.
- anterolateral fibres cross immediately in the anterior commissure of the cord to the opposite anterior and lateral white columns
- turn up towards brain via anterior spinothalamic and lateral spinothalamic tracts
- upper terminus of tactile signals: ventrobasal complex (mostly tactile signals)
- upper terminus of pain signals: retinacular nuclei of brain stem, projected to intralaminar nuclei of thalamus
35
Differentiate the modal specificities of the two spinothalamic pathway routes.
LATERAL SPINOTHALAMIC ROUTE
- A-delta fibers --> heat or cold
- C fibers --> dull pain and itch
ANTERIOR SPINOTHALAMIC ROUTE
C fibres --> coarse, non-discriminating touch
36
Where does decreased pain and temperature perception occurs when the lateral spinothalamic tract is damaged?
- on contralateral side
| - one or two dermatomes below
37
Give 4 influencing factors on how pain is perceived.
- situation
- emotion
- genetic susceptibility
- previous experience
38
Which type of receptor are nociceptors? What 3 stimuli excite them?
free nerve endings
- mechanical
- thermal
- chemical
39
Differentiate between the fast-sharp and slow-chronic pain pathways. Explain double pain sensations relative to these.
FAST-SHARP PAIN PATHWAY
- elicited by mechanical or thermal pain
- small A-delta fibres (6-30m/s)
SLOW-CHRONIC PAIN PATHWAY
- mainly elicited by mechanical pain
- C fibres (o.5-2m/s)
DOUBLE PAIN SENSATIONS
- sharp pain first from A-delta fibers--> immediate action or reaction
- slow pain second from C fibers --> stimulates person to try to relieve cause
40
What happens when you eat a chilli pepper?
capsaicin in chilli pepper
capsaicin mimics chemicals produced at sites of tissue damage --> activates Trp1 channel in nociceptor neurons --> influx of calcium and sodium --> depolarisation --> production of an action potential
41
What information does the spinocerebellar pathway carry and to where?
body's position and movements from muscle spindles, Golgi tendon organs and touch receptors
to vermis of cerebellum
42
How does the spinocerebellar tract differs from the other two ascending tracts ?
spinocerebellar tract: only two neurons along its length
| other ascending tracts: 3
43
Where are the cell bodies of the second order neurons from the spinocerebellar tract located?
dorsal horn of spinal cord
44
Compare dorsal and ventral tract neurons from the spinocerebellar tracts.
DORSAL TRACT NEURONS
- ascend ipsilaterally
- enter cerebellum via inferior peduncle
VENTRAL TRACT NEURONS
- ascend contraterally
- enter cerebellum via superior peduncle
45
Describe the aetiology, and symptoms of Freidreich's ataxia.
inherited disease caused by multiple repeats of a gene for protein Frataxin (responsible for iron metabolism in mitochondria)
spinocerebellar tract becomes increasingly ineffective:
- progressively uncoordinated arm and leg movements
- wide based reeling gait
- intention tremor
46
Give the 5 requirements of purposeful movement.
- goal or purpose
- activation of relevant movement
- feedback of movement
- refinement/correction of movement
- cessation on completion
47
Where is the motor cortex located?
occupies 1/3 of frontal lobes, anterior to central cortical sulcus
48
Describe the function of each area of the motor cortex.
PRIMARY MOTOR CORTEX
excites a specific movement (pattern of separate muscles)
PREMOTOR AREA
complex patterns of movement
SUPPLEMENTAL MOTOR AREA
- bilateral contractions
- background movement for other areas to add onto
49
Describe the path of the corticospinal tract.
cortex --> pyramids of medulla
majority cross in lower medulla --> lateral corticospinal tracts
those which do not cross --> ventral corticospinal tracts
mainly terminate on interneurons
50
What percentage of signals in the corticospinal tract originate from the somatosensory cortex?
40%
51
Which pathway of the corticospinal tract is conscious movement conducted through? and unconscious movement?
CONSCIOUS MOVEMENT
lateral pathways of corticospinal tract
UNCONSCIOUS MOVEMENT
ventromedial pathways of corticospinal tract
52
What kind of movements does the ventromedial pathway regulates?
control of posture and rhythmic movements associated with locomotion
53
Define posture and explain the mechanism the body uses to control it.
posture: position of a body and its part relative to each other --> a compromise between balance and movement
central command --> limb movement and postural adjustment
limb movement --> postural instability --> postural adjustment
54
What sensory inputs are integrated for posture control?
- muscle proprioceptors
- sense of balance derived from movements of the head relative to the Earth's gravitational field (vestibular apparatus)
- visual inputs
55
Which structures of the brainstem integrate the sensory inputs for posture control?
- retinacular nuclei
| - vestibular nuclei
56
What are the three pathways involved in posture? How do they work?
LATERAL VESTIBULOSPINAL PATHWAY
- facilitate extensor motor neurons and inhibit flexor neurons innervating the ipsilateral medial and axial muscles
- activate both alpha and gamma motor neurons --> enhanced muscle spindle-mediated stretch reflexes
--> increase the tone to antigravity muscles
MEDIAL VESTIBULOSPINAL PATHWAY
- controls head and eye movements together to maintain a steady gaze regardless of body movement
- unplanned head movements activate the vestibular apparatus --> projects to medial vestibular nucleus --> links info together and transmits signals to cranial nerves
RETICULOSPINAL PATHWAY
- sensory info from vestibular nuclei, cortical areas for colunatry movement, proprioception, vision... processed in brainstem's reticular formation
- pontine and medullary output for coordination of truncal and proximal muscle activity for primitive response
- also affects muscle tone in response to planned and coordinated motor activity
57
What are positive and negative signs regarding upper motorneuron lesions?
positive sign --> appearance of abnormal response
| negative sign --> loss of function
58
Describe the mechanism for non-specific binding of a drug in experiments.
in an experiment,
| excess drug compared to receptors --> drug binds to other sites of receptors without activating it
59
Define efficacy. Give one principle linked to efficacy.
efficacy: capacity of a drug to initiate a response from a receptor
the maximum response of a tissue can be obtained by occupying less than 100% of the receptors
60
Give the equation of the occupancy theory.
response = [occupied receptors]/[total number of receptors]
61
Two drugs have the same pD2. At the same concentration, one drug produces three times the effect that the other drug does. Which has the greatest affinity? And the greatest efficacy?
Greatest affinity --> neither (same pD2)
| Greatest efficacy --> the drug that produces the most effect
62
Give the equation of efficacy.
response = f([DR]/[RT])
63
What are spare receptors?
extra receptors inactivated when less than 100% of receptors are required to evoke a maximum response
64
What do partial agonists do to response intensity?
partial agonists can never reach full response
dampen the response of receptors to a full agonist by competing for receptors active site
65
Define competitive antagonist and give an equation.
a drug that interacts/binds reversibly with receptors to form a complex but this complex does not evoke a response
[D] + [R] + [A] [DR] + [AR]
some of the DR will elicit a response
no AR will evoke a response
66
What is the symbol used for the equilibrium dissociation constant for an antagonist? How can it be defined?
K(a)
concentration of antagonist that makes it necessary to add twice as much agonist to produce a response as would be needed in the absence of the antagonist
67
How does a competitive antagonist displace a log does-response curve? How do you calculate the ratio by which the drug concentration must be increased to overcome competition by the antagonist?
- displaced to the right
- same maximum response
Schild equation:
r = 1 + ([A]/K(a))
68
What value could you use to compare the affinity of a drug and a competitive antagonist?
pA2, calculated from K(a)
69
Give two other names for orthosteric inhibition.
allosteric inhibition, non-competitive inhibition
70
Which property(ies) of a receptor and of its drug does allosteric binding modify?
RECEPTOR
potentiated or inhibited
DRUG
- affinity
- efficacy
71
How does an irreversible competitive antagonist modify a log dose- response curve?
- slope decreased
| - maximum response to agonist decreased
72
Differentiate between negative affinity and negative efficacy modulation.
NEGATIVE AFFINITY MODULATION
increase in [D] needed to reach maximum response
NEGATIVE EFFICACY MODULATION
decrease in maximum response possible
73
What is the effect of an inverse agonist on a receptor's response? How is it modified in the presence of a competitive antagonist?
Dampened response
curve shifted to the right
74
Where would you find the recurrent branch of the median nerve lying?
superficially on distal border of flexor pollicis brevis
75
Name the two large branches of the radial artery that arise from after the anatomical snuffbox?
- princeps pollicis
| - radialis indicis
76
Which two fingers are moved by the two most superficial tendons of flexor digitorum superficialis?
middle and ring fingers
77
What are the two heads of adductor pollicis named?
oblique and transverse
78
Outline the process of formation of catecholamines.
tyrosine ---(tyrosine hydroxylase)---> DOPA rate-limiting step
DOPA ------> dopamine
dopamine -------> noradrenaline
noradrenaline -------> adrenaline
79
What are the two noradrenaline reuptake/upptake transporters? Why are they so important
NET in neurons for reuptake --> 75%
VMAT (vesicular monoamine transporter) in target cells or adjacent tissues for repackaging --> 25%
important because no equivalent of acetylcholinesterases for noradrenaline
80
Give one example of drug that affects each of catecholamine synthesis, release, uptake and metabolic degradation.
SYNTHESIS
methyldopa
RELEASE
amphetamines (sympathomimetics), clonidine (alpha 2 receptors)
UPTAKE
Net inhibitors: cocaine, tricylic antidepressants
METABOLIC DEGRADATION
MOA inhibitors
81
Where would you find most beta 3 adrenergic receptors?
in adipocytes
82
Give the main locations, cellular response and functional ANS response of adrenoreceptors alpha 1 and 2, beta 1 and 2.
ALPHA 1
- CV system, GI tract, GU system
- increase in IP3 and DAG
- mostly vasoconstriction, smooth muscle contraction (GI & GU)
ALPHA 2
- neurons
- decrease in cAMP
- decreased transmitter release
BETA 1
- heart and kidneys
- increase in cAMP
- increased cardiac rate and force (output), renin release
BETA 2
- lungs, smooth muscle, skeletal muscle
- increase cAMP
- bronchodilation, relaxation of visceral smooth muscle, vasodilation in smooth muscle, tremor
83
Which medication would you give to someone with nasal congestion caused by an upper respiratory tract infection, and why? What are the risk of taking too much?
Phenylephrine
alpha 1 agonist --> vasoconstriction of airway blood vessels
risks: general vasoconstriction leading to an increase in BP
84
Compare and contrast Salbutamol and Salmeterol
both beta 2 agonists used for the treatment of asthma
side effects include muscle tremors and cardiac arrhythmias
SALBUTAMOL
- short-acting (SABA)
- used for treatment of acute crises of asthma, and also used to delay delivery in premature labour
SALMETEROL
- long-acting
- used for chronic treatment of asthma and COPD
85
How does sympathetic stimulation increase the mean arterial BP?
- increases cardiac output (beta 1 receptors: increases heart rate and stroke volume)
- increases total peripheral resistance (alpha 1 receptors: vasoconstriction)
86
What condition would you prescribe Dobutamine for? What is the mechanism of action of the drug?
cardiogenic shock --> damaged heart unable to supply enough blood to organs
dobutamine = beta 1 agonist --> increases heart rate and force --> increases perfusion
87
Which 4 medications could you prescribe for hypertension? What adrenergic receptor does each affect?
PRAZOSIN
alpha 1 antagonist
PROPANOLOL
ATENOLOL
beta 1 antagonists
CLONIDINE
alpha 2 agonist
88
Why can some beta-blockers be problematic in asthmatic? What condition other than hypertension are they sometimes used to treat?
non-cardioselective beta-blockers have both beta 1 and 2 antagonistic effects
off-target effects on beta 2 keeps beta 2 receptors from activating and elicit bronchodilation, necessary for asthmatic to be able to breathe when in crisis
anxiety
89
Which medication can be prescribed for treatment of both cardiac arrest and anaphylactic shock?
adrenaline
90
What is benign prostatic hyperplasia? Give the names of two drugs that can be used to treat this condition.
swollen prostate causing problems with passing urine
- prazosin
- tamsulosin
91
Name 3 agonists of alpha 2 adrenergic receptors, and 3 antagonists.
AGONISTS
- noradrenaline
- adrenaline
- clonidine
ANTAGONISTS
- phentolamine
- prazosin
- carvedilol
92
Contrast haemostasis and thrombosis.
HAEMOSTASIS
arrest of blood loss from damaged blood vessels
THROMBOSIS
unwanted formation of a haemostatic plug within the blood vessels or heart
93
Give an example of a genetic coagulation defect, and 3 of an acquired one.
GENETIC
haemophilia
ACQUIRED
- liver disease
- vitamin K deficiency
- ingestion of oral anti-coagulant
94
What are the respective names of the natural and synthetic preparations of vitamin K?
natural --> phytomenadione
synthetic --> menadiol sodium phosphate
95
What is the role of vitamin K in coagulation? and its clinical uses?
co-factor in post-translational processing of factors II, VII IX and X
clinical uses:
- treatment/prevention of bleeding from excessive oral anticoagulant use
- prevention of haemorrhagic disease of newborn
- vitamin K deficiencies in adults
96
Which oral anticoagulant drug family does not require monitoring? Name two drugs that belong to this family.
direct inhibitors of factor Xa
rivaroxaban, apixaban
97
What are the two ways doctors go around the long onset of Warfarin?
- use a loading dose to increase plasma concentration
| - temporary heparin treatment
98
Give two factors that would increase the effect of warfarin.
- liver disease
- broad-spectrum antibiotics
- drugs which impair platelet function
- drugs which displace warfarin from plasma albumin
- agents that inhibit microsomal enzymes in the liver
99
What are the advantages of LMWH?
- doesn't require monitoring
| - longer-acting
100
Where does heparin naturally occur?
- mast cells
- plasma
- endothelial cells
101
The activity of what enzyme does heparin support?
antithrombin III
102
Which anticoagulants has for main side effect haemorrhage, without antidote?
rivaroxaban, apixaban
103
Which drug inhibits both P2Y12 purinergic receptors and ADP-induced platelet aggregation?
clopidogrel
104
On which bonds does plasmin act?
ARG-LYS
105
Describe the mechanism of action of streptokinase.
activates enzymatic activity of plasminogen by inducing a conformational change
106
Give two sources of alteplase.
- in vivo by endothelial cells
| - recombinant technology
107
Which antiplatelet drug is said to be clot-selective?
alteplase
108
What medications would you give with 4 to 6hrs of onset of acute MI?
fibrinolytic agents (streptokinase) + aspirin
109
Give 6 routes of entry for pathogens. Give one example of disease for each.
- airway (influenza, menigococcal meningitis)
- GI tract (typhoid fever, diarrhea, salmonella)
- GU (syphilis)
- external surface (athlete's foot)
- wounds or abrasions (anthrax, tetanus)
- insect bites (yellow fever, malaria, Lyme disease)
110
Give the names and the time-length of each phase of response to initial infection.
innate immunity: 0-4hrs
early-induced response: 4-96hrs
adaptive immune response: >96hrs
111
Give the three barriers to infection, and two examples for each
MECHANICAL
- tight junctions
- air and fluid flow across epithelium
- movement of mucus by cilia
CHEMICAL
- fatty acids on skin
- enzymes in saliva, tears, sweat...
- low pH in stomach
- antibacterial peptides
MICROBIOLOGICAL
- normal flora offering competition for nutrients and attachment
- normal flora producing antibacterial substances
112
Give three examples of bactericidal effects and agents produced by phagocytes.
- acidification
- toxic oxygen derived products
- toxic nitrogen oxides
- peptides
- enzymes
- competitors
113
What is the common progenitor of all cellular elements of the blood?
haematopoietic stem cell in bone marrow
114
What percentage of circulating WBC do neutrophils represent? and of polymorphonuclear cells?
WBC: 70%
| PMN cells: 99%
115
Name three types of molecules granules of eosinophils contain.
- histamine
- peroxidase
- RNases
- DNases
- lipase
- plasminogen
- major basic protein
116
What chemicals do basophils secrete upon activation?
- histamine
- proteoglycans
- leucotrienes
- cytokines
117
What are the three effects or release of interferons by a virus-infected cell?
- induce resistance to viral replication in all cells
- increase MHS class I expression and antigen presentation in all cells
- activate Natural Killer cells to kill virus-infected cells
118
Give two differences between NK cells and CD8 T cells.
- NK cells not antigen specific; CD8 T cells are
| - CD8 T cells undergo lengthy clonal expansion in lymph nodes when virus is detected; NK cells don't
119
How do NK cells make the difference bewteen a healthy cell and a virus-infected cell?
presence or absence of MHC class 1 receptor
many infections lead to down regulation of MHC class 1
120
What are the three pathways leading to complement activation?
CLASSICAL PATHWAY
antibody binds to specific antigen on pathogen surface
LECTIN PATHWAY
mannose-binding protein binds to pathogen surface
ALTERNATIVE PATHWAY
pathogen surface creates local environment conducive to complement activation
121
What are the three end-points of complement activation?
- recruitment of inflammatory cells
- opsonization of pathogens, that facilitates uptake and killing by phagocytic cells
- direct lysis and death of pathogens
122
What are the 5 complements that participate in assembly of a membrane attack complex? What cell-surface protein intervenes to prevent final assembly on host cells?
C5b, C6, C7, C8, C9
CD59
123
What is meant by naive B cells?
B cells that have not met antigen
124
What are germinal centers on lymph nodes?
B cells growing in size during an immune response
125
What are the respective roles of red pulp and white pulp of the spleen?
RED PULP
site of RBC destruction
WHITE PULP
lymphoid tissue that filters the bloodstream
126
What property of B cells relate to the secondary response to infection by the same pathogen?
memory cells --> inactivated B cells sit in lymph nodes until the next infection from the same pathogen
127
How many types of antibodies can a B cell produce?
one
128
How are antibody structured?
4 intertwining polypeptide chains:
- 2 identical heavy chains, disulfide bonded to each other
- 2 identical light chain
each H chain disulfide bonded to a L chain
two different regions:
- a variable region (attaches to antigen)
- a constant region (attaches to cell)
129
How can antibody be cleaved?
- cleavage between Fab and Fc region
| - cleavage between F(ab)2 and part of Fc
130
What are the three shapes of antigen-binding regions of antibodies?
- pocket
- groove
- extended surface
131
What are the mechanisms that explain antibody diversity (high variability in V regions of light chains)?
Somatic diversification theory:
during B cell development:
- chromosomal rearrangement
- junctional diversity
- different combinations of H and L chains
after B cells have become antigen activated:
- somatic hypermutation by affinity maturation
132
Name the 5 classes of antibodies.
IgG, IgM, IgD, IgA, IgE
133
How do transmembrane and secreted IgM differ?
transmembrane IgM has a transmembrane region, and secreted IgM doesn't
134
Why is there usually no IgE found free in plasma?
stored in mast cells
135
Give two antibody multimers. What protein is key to the formation of such structures?
- pentameric IgM
- dimeric IgA
J chain
136
Give three functions of antibodies.
- blocking of virus binding to receptor on host cell
- blocking toxins from binding to cell-surface receptors
- opsonization
137
What is the role of IgE?
IgE triggers the release of granules contents (including histamines) from mast cells
138
What kidney condition has high levels of antibody-antigen complexes as a major cause?
glomerulonephritis
139
What type of cells are fused with activated B cells in monoclonal antibody production?
myeloma cells
