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Phase 2a Gold Standard > ICS - Immunology > Flashcards

ICS - Immunology Flashcards

1
Q

What do toll like receptors respond to?

A

PAMPs - Pathogen
DAMPs - Damage

Associated Molecular Patterns

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2
Q

Important TLRs (apparently)

A

2,4,5,7,9

2- G+ and TB (extracellular)
4 - lipopolysaccharides (G-) (extracellular)
5 - Flagellin (extracellular)
7 - Single strand RNA (intracellular)
9 - unmethylated CPG DNA (intracellular)

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3
Q

Which TLRs are intracellular

A

3,7,8,9

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4
Q

All TLRs (1-11) and what they recognise

A

*2 - gram positive + TB
3 - viral dsRNA
*4 - Lipopolysaccharides (G-)
*5 - Flagellin
6 - Lipoteichoic acid (G+)
*7 - single stranded RNA
8 - DSRNA (G+)
*9 - CPG (non methylated) DNA (bacteria)
11 - bacteria (urogenital pathogens)

1,2,6 - bacterial cell wall components
3 - dsRNA
4 - G- LPS
5 - flagellin
7 - ssRNA
9 - unmethylated CpG

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5
Q

Innate vs adaptive immunity

A

Innate
- Non specific
- Resistance not improved by reinfection
- Instinctive
- Rapid response
- Phagocytes and natural killer cell
- No memory

Adaptive
- Specific “acquired” immunity
- Resistance improved by repeat infection
- Slower response
- Requires lymphocytes (T&B)
- Memory

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6
Q

Clinical indications of an allergic reaction
(Skin, Airways, GI)

A

Skin - Swelling, itching, reddening
Airways - Excessive mucus production, bronchoconstriction
GI - Abdominal bloating, vomiting, diarrhoea

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7
Q

What stem cell do blood cells originate from

A

Haematopoietic pluripotent stem cell

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8
Q

What are the 3 ways the complement system destroys pathogens

A

Innate immunity

  1. Direct lysis - (membrane attack complex) - Group of complements make a hole in pathogen
  2. Opsonisation - (C3b) antigen coated with complement that makes it easier to phagocytose
  3. Increase inflammation - (C3a and C5a)
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9
Q

Neutrophil properties

A

65% of blood
Lifespan: 6 hours - 12 days
Contain primary lysosomes and secondary granules which secrete toxic substances to kill microbes
Key role in innate immunity and inflammation

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10
Q

Monocyte properties

A

Lifespan: months
Innate (phagocytosis) and adaptive (antigen presentation) roles
Differentiate into macrophages in tissue

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11
Q

Macrophage properties

A

Lifespan: Months/years
Kupffer cells in liver, microglia in brain
innate (phagocytosis) and adaptive (antigen presenting) role
First line non self recognition

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12
Q

Macrophage properties

A

Lifespan: Months/years
Kupffer cells in liver, microglia in brain
innate (phagocytosis) and adaptive (antigen presenting) role
First line non self recognition

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13
Q

Eosinophil properties

A

Lifespan: 8-12 days
Contain major basic protein (MBP) toxin, which activates neutrophils and induces histamine release
Granules stain using eosin (red/pink)
Often seen in parasitic infection

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14
Q

Basophil properties

A

Lifespan: 2 days
Express high affinity IgE receptors, which cause degranulation and release of histamine.
Similar to mast cells (mast cells fixed, basophils circulate in blood)
Granules stain using haemotoxylin (blue/violet)

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15
Q

T lymphocyte (t cell) properties

A

Hours-years
Originate in bone marrow but mature in thymus
Recognise antigens displayed by antigen presenting cells, which they bind to with t cell receptors.
Produce cyotkines
Found in blood, lymph nodes, spleen

T helper 1&2 (CD4)
Cytotoxic T cell (CD8)
T reg

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16
Q

Natural killer cells

A

Express CD56
Recognise and kill virus infected cells and tumour cells by apoptosis

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17
Q

Primary vs secondary lymphoid organs

A

Primary - Bone marrow (immune cell origin, b cell maturation site), thymus (t cell maturation site)
Secondary - Lymph nodes, spleen (Removal site of RBC and antibody coated bacteria)

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18
Q

Physical and chemical barriers in innate immunity

A

Physical - skin, mucus, cilia
Chemical - Lysozyme in tears, stomach acid

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19
Q

What are antigen presenting cells and 2 functions?

A

E.g. dendritic cells
Present foreign antigens to T helper cells.

Stimulates Th proliferation
or B cell production

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20
Q

Explain TLR 4

A

TLR activated by LPS on gram negative bacteria (endotoxin)
Trigger immune response (activate complement, cytokine release (TNFa, IL1,6), phagocytosis)

21
Q

Explain Thymic tolerance

A

Thymic tolerance/selection used to see if immature T cells are functional. Any failed selection results in apoptosis.

+ selection (self recognition) - CD8 (Tc) binds to MHC-I, CD4 (Th) binds to MHC-II with moderate strength; recognise self. Allowed to survive.

  • selection - If TCR (T cell receptor) on t cell recognises and binds to MHC-I or II (producing immune response to self) it has to be phagocytosed. TCR shouldnt interact with self

allocation - If immature T cell interacts with MHC-1: CD8 upregulated and becomes Tc cell
If reacts with MHC-2: CD4 upregulated, becomes Th cell

22
Q

CD8 T cell function

A

Cytotoxic T cells interact with MHC-I

Direct killers - Secrete Perforin or express FAS to trigger apoptosis

23
Q

CD4 T cell function

A

T Helper cells that interact with MHC-II

TH1 - IFNy - Activate NK cells and macrophages (innate immunity)

TH2 - IL4 - Activate B cells to differentiate into plasma cells (adaptive immunity)

24
Q

Where are B cells produced and where do they mature

A

Both in bone marrow

25
Q

Explain B cell activation

A

Th2 is activated by antigen presenting cell (dendritic cell) binding and MHC-II interactions.

It then releases IL 4 (causing B cell proliferation “clonal expansion”) and IL 5 (causing B cell differentiation into plasma cells which produce immunoglobulins)

26
Q

Give a brief overview of IgG

A

Most abundant in blood
Key in secondary immune response (marker of immunological memory)

27
Q

Give a brief overview of IgA

A

Most abundant in total body. Found on mucosal linings, in colostrum and in breast milk. Forms dimer

28
Q

Give a brief overview of IgM

A

First Ig released in adaptive response

Forms pentamer

29
Q

Give a brief overview of IgE

A

Found in type 1 hypersensitivity (anaphylaxis)

Activates mast cell/basophil degranulation

30
Q

Give 3 functions of MHC molecules

A

Ensure T cells recognise self (positive selection)
Check T cells can confer immunity and dont cause autoimmunity (negative selection)
Confer autoimmunity to HLA (human leukocyte antigen) related inherited autoimmune conditions

31
Q

Give the genes that cause these autoimmune conditions

Spondyloarthropathies
T1DM
Coeliac
SLE

A

All found on chromosome 6
Spondyloarthropathies: HLA-B27
T1DM: HLA-DR2DQ3
Coeliac: HLA- DQ2 (or DQ8)
SLE: HLA B8

32
Q

Explain type 1 hypersensitivity with examples

A

IgE mediated (anaphylaxis)

IgE binds to mast cell/basophil causing degranulation and histamine release.

E.g. atopy (asthma, hay fever, rhinitis)

33
Q

Explain type 2 hypersensitivity with examples

A

Antigen-antibody complex

IgG/IgM binds to antigen, activating MAC (complement) at SITE OF BINDING

E.g. Goodpastures, pernicious anaemia, rheumatic fever

34
Q

Explain type 3 hypersensitivity with examples

A

Immune complex deposition at sites away from binding

IgG/IgA bind to antigen and activate complement at site of deposition

E.g. SLE, post strep glomerulonephritis, IgA glomerulonephritis

35
Q

Explain type 4 hypersensitivity with examples

A

T cell mediated w/ delayed response

Th1 activated by APC, causing cytotoxic killing occurs around body

E.g. Type 1 diabetes mellitus, TB, MS, Guillain barre

36
Q

Describe patient presentation of anaphylaxis

A

Severe hypotension
Tachycardia
Dyspnoea
Pale
Cold extremities
Puffed up face and tongue
Pruritus/itching
Central cyanosis

37
Q

Explain treatment algorithm for anaphylaxis

A

1: ABCDE
Airway - can they breathe
Breathing - Rapid, wheezy, low SpO2? (<92%)
Circulation - pale, cold, clammy, low BP, capillary refill time?
Disability - Confused/comatose, movement
Exposure to antigen

2 - 500mcg IM adrenaline

38
Q

Effects of histamine

A

Vasodilation, increased permeability (H1 receptor), bronchoconstriction facial flush, pruritus, swollen tongue/face

39
Q

Describe immune tolerance

A

Non responsiveness to specific antigens to prevent self immune response

Central - occurs in the thymus/bone marrow during T/B cell maturation

Peripheral - Occurs after mature cells have been released into blood. Works to prevent autoimmunity, in secondary organs such as spleen.

40
Q

Define autoimmunity

A

Pathological immune response against self either through faulty immune tolerance or molecular mimicry

41
Q

Give examples of organ specific autoimmunity

A

T1DM - pancreas (b cells)
MS - Oligodendrocytes of CNS
Pernicious anaemia - parietal cells of stomach
Hashimoto’s - antibodies against TPO
Graves - Antibodies against TSH receptors

42
Q

Give examples of non organ specific autoimmunity

A

SLE - affects DNA (ANA)
Autoimmune anaemia affects RBC
Autoimmune thrombocytic purpura affects platelets

43
Q

Define immunodeficiency

A

The reduced ability of the body to fight infection or disease

44
Q

Give some causes of immunodeficiency

A

Primary (Inherited): T/B cell defect/deficiency, IgA deficiency, CVID, SCID

Secondary (Acquired):
HIV, malnutrition, cancer, diabetes mellitus, chemotherapy, leukaemia, myeloma

45
Q

Patterns of immunodeficiency

A
  • Decreased CD4/T helper cells in HIV, leading to increased susceptibility to disease
  • Deficient B cells (decreased plasma cells/antibodies)
  • Neutrophil/macrophage deficiency (less phagocytosis/acute inflammation)
  • Complement deficiency (innate immunity doesnt work as well)
  • hyposplenism (lack of RBC recycling and killing of encapsulated bacteria)
46
Q

Define active immunity with natural and artificial example

A

Active immunity involves:
Ig production, immunological memory and response largely secondary.

Natural: Body encounters pathogen, producing antibodies and memory cells

Artificial: Vaccine mimics encountering pathogen, stimulating Ig production

47
Q

Define passive immunity, with natural and artificial example

A

Passive involves Ig’s passed directly to host with no memory and a primary response

Natural: maternal antibodies passed to feeding baby through breast milk/colostrum

Artificial: Antivenom, or Ig injection/transfusion

48
Q

What are the aims of a perfect vaccine

A
  • Achieve long term protection from small number of immunisations
  • Stimulate BOTH B and T cells
  • Induce memory B and T cells
  • Stimulate protective IgG and IgA production
49
Q

Active vs passive immunity

A

Active
- IgG production
- Immunological memory
- Secondary response

Passive
- IgG passed to host
- No memory
- Primary response

Phase 2a Gold Standard (29 decks)

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