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MD2002 > WEEK 5 > Flashcards

WEEK 5 Flashcards

1
Q

All the cells of the immune response come from the same progenitor cell. What is said cell called?

A

Hematopoetic stem cell

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2
Q

Name, and describe, the various stages of the three different types of immune response elicited by the body.

A
  1. Innate immunity: immediate (0-4hrs)
    - infection
    - recognition by preformed non specific effectors
    - removal of infectious agent (ia)
  2. Early induced response: early (4-96hrs)
    - infection
    - recruitment of effector cells
    - recognition and activation of effector cells
    - removal of ia
  3. Adaptive immune response
    - infection
    - transport of antigen to lymphoid organs
    - recognition by naive B & T cells
    - clonal expansion of effector cells
    - removal of ia
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3
Q

What happens to microorganisms once across the epithelial barrier?

A

They are recognised & ingested by mononuclear phagocytes or macrophages

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4
Q

Describe each of the following (i) monocyte (ii) neutrophil (iii) eosinophil (iv) basophil.

A

(i) one of 3 types of phagocytic cel of immune system
- they circulate the bloodstream, becoming macrophages when in tissue.
(ii) (PMN) - most numerous & important cell of innate response
- are v. short lived (2 days)
(iii) (PMN) - parasite defence. Important in getting rid of gut pathogens
(iv) (PMN) - function is similar to that of eosinophils & mast cells. They are the least common PMN.

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5
Q

What are mast cells?

A

granules.
When releases, they release a number of substances that affect the vascular system
ie. IgE mediated triggering in allergies

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6
Q

Name the two types of lymphocytes and what they produce.

A

B cells = produce antibodies

T cells = cytotoxic T cells (CD8) OR helper T cells (CD4)

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7
Q

What is the function of dendritic cells?

A

most important immune cell
they bridge the gap between the innate and adaptive immune response
are specialised in antigen uptake and presentation

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8
Q

What are NK cells? What is their role within the body? How do they stop themselves from destroying healthy cells?

A

Large granular lymphocytes
Recognise virally infected cells non-specifically
Play and early defence role against viral infection
Have receptors on their cell surface to prvent them from destroying healthy cells.

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9
Q

What is the difference between NK cells and CD8 cells ? (HINT: there’s two)

A
  • NK cells aren’t antigen specific

- NK cells don’t require clonal expansion of T cells in lymph nodes when the virus is detected.

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10
Q

What are the 3 pathways of the complement cascade? Describe each one.

A
  1. Classical pathway:
    - initiated by activation of the C1 complex
    - antibodies binding onto the surface of bacteria
    - C1Q acts with the antibody
    => triggering the classical pathway
  2. Lectin pathway
  3. Alternative pathway:
    - cause by spontaneous hydrolysis of serum C3
    - this binds to factor B
    - factor B is cleaved by factor D into Ba and Bb
    - the resulting soluble C3 convertase cleaves C3 -> C3b
    - C3b binds to membranes and acts to increase phagocytosis
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11
Q

How is the membrane attack complex (MAC) assembled? What can prevent the final assembly of MAC?

A

It is comprised of C6, 8, 9 which form a pore
=> the internal contents of bacteria leak out & bacteria dies
CD59 - at the C8 -> C9 stage

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12
Q

What is an atheroma?

A

degeneration of the walls of the arteries caused by accumulated fatty deposits and scar tissue, and leading to restriction of the circulation and a risk of thrombosis.
- the fatty material which forms deposits in the arteries.

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13
Q

What are the risk factors associated with atherosclerosis? (HINT: there’s 7)

A

Age: prime age = 40-60
Sex: males are more predisposed compared to woman PRE menopause
Genetics: diabetes, hypertension
Hyperlipidaemia: increased cholesterol (dietary factors)
Hypertension: more likely
Smoking
Diabetes Mellitus

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14
Q

What is the pathogenesis of atherosclerosis? (HINT: there’s 6)

A 
1. Chronic Endothelial Injury
increased:
-􏰃Endothelial permeability
􏰃-Leukocyte adhesion
-Monocyte adhesion and migration
2. Role of lipids
 Hyperlipidaemia (LDL cholesterol)
– Impairs endothelial function
– Accumulates within intima
– Causes oxidative modification of LDL:
Ingested by macrophages via SCAVANGER receptors = foam cells
3. Role of macrophages
Engulf oxidised LDL = foam cells 
Secret IL1, TNF, MCP1 and growth factors
FATTY streak
4. Smooth muscle proliferation
Collagen and Extracellular matrix deposition
=> Fattystreak -> Mature fibro-fatty Atheroma
5. Fibro-lipid plaque formation
6. Injury to plaque: thrombus formation
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15
Q

Describe the morphology of atherosclerosis. Where do they develop? (name a few examples)

A 
Atheromatous plaque
> patchy & raised, white to yellow
> lipid core, fibrous cap
Abdominal aorta
coronary arteries
popliteal arteries
descending thoracic aorta
internal carotid artery
vessels of circle of willis
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16
Q

What are the complicated lesions that can occur in atherosclerosis?

A 
calcification
rupture/ulceration
haemorrhage
thrombosis
aneurysmal dilation
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17
Q

What results in complications within atherosclerosis?

A

thrombosis
calcification
aneurysmal dilation
ischaemic events

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18
Q

Describe the primary and secondary preventions of atherosclerosis.

A 
Primary (preventing atheroma)
- stop smoking
- control hypertension
- weight loss
- lower total LDL (statin)
- reduce calorie intake
Secondary (one complication has arisen)
- prevent complication
- anti-platelet drugs in thrombosis
- lower blood lipid levels
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19
Q

What is haemostasis?

A

The arrest of blood loss from damaged blood vessels via:

  • vascular constriction
  • formation of a platelet plug
  • formation of a blood clot (as result of coagulant)
  • growth of fibrous tissue into blood clot to close the hole permanently
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20
Q

What is drug therapy used for?

A

to modify:
- blood clotting
- platelet adhesion & activation
and to affect processes involved in fibrin removal

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21
Q

What are the two ways in which you can develop coagulation defects?

A 
Genetically
- haemophilia
Acquired
- e.g. liver disease, vit K deficiency
- treat with either natural or synthetic vitamin K
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22
Q

What is the mechanism of action of vitamin K?

A

acts as a co-factor in the post translational processing of factors II, VII, IX, X

23
Q

What are the clinical uses of vitamin K?

A
  1. treatment/prevention of bleeding from excessive oral anticoagulant use
  2. prevent hemorrhagic disease of newborns
  3. Vit K deficiencies in adults
24
Q

What factors (i) increase the effect and (ii) decrease the effect, of anticoagulants?

A 
(i) decreases in availability of vitamin K
broad spectrum of antibiotics
liver disease
drugs that impair platelet function
(ii) drugs thatincrease drug metabolism
oral contraceptive
25
What is warfarin?
it prevents the reduction of vitamin K (Vit K antagonist) it takes many hours to act due to having to degrade factors already formed a side effect can be haemorrhage => patients have to be monitored (PT/INR)
26
Name, and describe, the two types of injectable anticoagulants.
1. Heparin (e.g. Dalteparin) - naturally occurring - found in mast cells, plasma & endothelial cells - immediate actin 2. Heparan sulphate (not used therapeutically) - occurs extracellularly - important endogenous anticoagulant
27
What is the mechanism of action of heparin?
Its activity is related to its electronegative charge Acts mainly on fibrin formation - it acts on ATIII & other serine proteases in the coagulation cascade (XIIa, XIa, IXa, Xa) - ATIII forms a 1:1 complex with thrombin - heparin accelerates the rate of this inhibition
28
What are the two direct Xa inhibitors? Describe them.
``` Rivaroxaban or Apixaban - orally active - no monitoring needed - few hours to act - effects last 8-12 hours (Xa activity normal after 24hrs) BUT there's no antidote ```
29
What is the role of antiplatelet drugs? Name, and describe, two.
Decrease platelet aggregation & inhibit thrombus formation 1. Aspirin - inhibits cyclooxygenase 2. Clopidogrel - inhibit P2Y(12) purinergic receptors
30
What is fibrinolysis?
set in motion when the intrinsic coagulation system is acitvated it involves the generation of plasminogen activators (plasminogen = proenzyme) plasminogen activators release the active enzyme plasmin from its plasminogen precursor.
31
What is plasmin?
Trypsin like enzyme acting on ARG-LYS bonds - digests fibrin and other blood proteins (factors II, V, VII) - acts locally on fibrin meshwork of clot - when it escapes into circulation it is inactivated by inhibitors
32
Name a fibrinolytic agent and a tissue plasminogen activator (TPA). Describe each respectively.
1. Streptokinase - non enzymatic - acts indirectly - forms stable complex with plasminogen and activates the enzyme activity of plaminogen by inducing a conformational change 2. Alteplase - synthesised in vivo by endothelial cells - can be made by recombinant technology - its enzymatic activity is more enhanced int he presence of fibrin bound plasminogen than plasma plasminogen => clot selective.
33
What are some of the therapeutic uses of anticoagulants?
Venous TE | - DVT, PE, TE from AF, prosthetic heart valves, clotting during kidney dialysis
34
Why are antiplatelet and fibrinolytic agents used? Give named examples.
Fibrinolytic plus aspirin: - acute myocardial infarction - former needs to be given within 4-6 hours of onset Aspirin: - can reduce risk of occlusive CV disease in patients who are already diagnosed as being at risk
35
What are the predominate locations of AChR's? (muscarinic and nicotinic)
``` 1. Nicotinic: NMJ sympathetic ganglia parasympathetic ganglia CNS 2. Muscarinic: - parasympathetic target organs - sweat glands (sympathetic) - vascular smooth muscle - CNS ```
36
Where else are various muscarinic receptors found apart from the ANS?
M1, 2, 4, 5 are also found in the CNS | M3 is found on vascular endothelial & smooth muscle cells
37
What is the main locations and functional response of (i) M1 (ii) M2 (iii) M3?
(i) NEURAL: Autonomic ganglia glands => gastric secretion (ii) CARDIAC: Heart (atria) => cardiac inhibition (iii) GLANDULAR/SMOOTH MUSCLE: exocrine glands, smooth muscle BVs => gastric salivary secretion, GI smooth muscle contraction, ocular accommodation, vasodilation
38
What is the general problem with muscarinic antagonists? How is this problem overcome?
SELECTIVITY - very few differentiate between different subtypes - MAChR widespread => side effects This problem is overcome by - controlling the rout of administration and distribution
39
Describe NA release and the various factor affecting this process. What is NA's equivalent to ACh.E?
Facilitated by Ca2+ - feedback of NA is done by alpha2 adrenoreceptors on the presynaptic terminal => decrease in Ca2+ influx = less NA released There is no equivalent => 75% is recaptured by neurons and 'repackaged' by VMAT (vesicular monoamine transporter)
40
List the various drugs which affect noradrenergic neurons?
1. Affect catecholamine synthesis - methyldopa 2. Affect catecholamine release - indirectly acting sympathomimetrics amphetamines by acting on the alpha 2 adrenoreceptor - clonidine 3. Inhibitors of catecholamine uptake - NET inhibitors = cocaine, tricyclic antidepressants 4. Inhibitors of catecholamine metabolic degradation - monoamine oxidase inhibitors (anti-depressants)
41
Where do B cells originate from?
bone marrow - mainly the shafts of long & flat bones | - found in lymph nodes
42
What is a naive B cell?
One which has not yet met an antigen | they circulate from the blood to the peripheral lymphoid tissue = main site of antigen encounter
43
Within a lymph node, what is contained in the cortex and in the medulla?
``` Cortex = outer section of B cells Medulla = macrophages & antibody secreting B cells ```
44
Where are many immune cells located? How do they enter into said location compared to how they enter into lymph nodes?
The spleen | They enter via bloodstream rather than via lymphatics
45
Compared to the primary response, what are the benefits of the secondary response?
faster can produce more antibodies doesn't prevent you from making a response to another antigen
46
What are the basic features of antibodies (Ab)? (i.e. expression, function, structure)
Expressed as either membrane bound or secreted forms B cells express a single Ab specificity only Ab's have 2 separate functions: 1. bind to the pathogen that elicited its production 2. recruit other cells/molecules that lead to the clearance/destruction of the pathogen Made of 2 H chains and 2 L chains Disulfide bonds L chains can be either lambda or kappa (NOT BOTH)
47
How is antigen specificity determined?
by 3 hypervariable loops | the final specificity is determined by a combination of loops from the light and heavy chains (NOT either alone)
48
What 3 ways can antigens bind?
(a) small peptide bound pockets (b) extended peptide from HIV protein bound in groove (c) extended surface interaction
49
How is Ab diversity created?
1. rearranging multiple gene segments 2. Junctional diversity 3. Different combinations of H and L chains 4. Somatic hypermutation - this occurs after B cells have become antigen activated in the lymph node
50
What is somatic hypermutation?
during the course of an immune response, mutations accumulate in the V regions of H and L chain genes. Some will bind to the antigen better and these cells are selected to bind and secrete antibody = AFFINITY MATURATION
51
What are the 5 classes of antibody and how are they defined?
IgG IgD IgA IgM IgE | defined by their H chain
52
How do cells get rid of their initial expression of IgM?
After antigen stimulation they can secrete as soluble version of the same IgM - made by alternative mRNA processing Cells also undergo isotope switching where the IgM H chain is swapped for IgG etc
53
What is monoclonal Ab? List some and give their uses (3)
powerful tool for research, diagnosis, and maybe treatment 1. Infliximab - anti tumour necrosis factor - rhematoid arthritis, psoriasis, inflammmatory bowel disease 2. Herceptin - anti HER2 - can block and lead to destruction of breast tumour cells (only ones which express high levels of HER2) 3. Gleevac - anti tyrosine kinase - effectuve against chronic myeloid leukemia
54
What are antibody-antigen complexes important for? What high levels of said complex result in?
important mechanism for clearing soluble antigens - taken up by phagocytes high levels of the Ab-Ag complexes are prevalent in some auto immune diseases (triggering the complement cascade) e.g. glomerulonephritis

MD2002 (17 decks)

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