immune responses Flashcards

1
Q

type 1 hypersensitivity , which immune components are involved

A

IgE

mast cells

basophils

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2
Q

examples of type 1 conditions

A

anaphylaxis

asthma (allergic)

allergic rhinitis (hayfever)

food and drug allergies

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3
Q

describe what happens in type 2 hypersensivity

A

IgM and IgG bind to self-cells causing them to be destroyed by immune cells (NK cells or complement)

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4
Q

cells involved in type 2 hypersensivity reactions

A

IgM, IgG

component

NK cells

cytotoxic

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5
Q

examples of type 2 hypersensitivity

A

AIHA

good pastures (Anti-GBM)

graves

myathensia gravis

rheumatic fever

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6
Q

most abundant WBC

A

neutrophils

short lifespan 6-8 hours

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7
Q

neutrophils play a main role in which part of the immune system?

A

innate immune system - immediate response to bacterial infections

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8
Q

explain type 3 hypersensivity reactions

A

complexes

inmmune complexes form (antigen-antibody) and are deposited in tissues

causing inflammaiton and tissue damage

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9
Q

cells involved in type 3 hypersensitivity responses

A

IgG

immune complexes

complement

neutrophils

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10
Q

examples of type 3 hypersensitivity conditons

A

SLE

RA

Post-streptoccal GN

Vasculititis - e,g, polyarteritis nodosa

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11
Q

describe type 4 hypersensitivity

A

DELAYED

T-cells release cytokines

activate macrophages and cause tissue damage OVER TIME

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12
Q

cells involved in T4 hypersensivity

A

T-cells CD4 and CD8

macrophages

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13
Q

comon T4 hypersensivity conditions

A

T1DM

MS

Contact dermatitis - poision ivy

TB - skin (mantoux test)

Crohns disease

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14
Q

: Fast allergic reactions (IgE-mediated) → anaphylaxis, asthma.

what response

A

T1

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15
Q

Antibody-mediated cell destruction (IgG/IgM) → hemolytic anemia, Graves’ disease.

what response?

A

T2

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16
Q

Immune complex-mediated inflammation → lupus, rheumatoid arthritis.

A

Type 3

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17
Q

T-cell-mediated delayed response → type 1 diabetes, multiple sclerosis.

A

type 4

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18
Q

what are the two phases of T1 hypersensitivity response

A
  1. Sensitization Phase (First Exposure to Allergen)
  2. Effector Phase (Subsequent Exposure & Histamine Release)
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19
Q

dendritic cells or macrophages are APC

a. true
b. false

A

a. true

APCs process the allergen and present it on their surface using MHC class II molecules.

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20
Q

r

responsible for generating most fever symptoms

A

IL-1

major enodgenous pyrogen

sereted by macrophages -to stimulates, T/B cellls and neutorphils

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21
Q
A
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21
Q

pyogenic

A

refers to anything that produces pus or is associated with pus formation

-> indicates bacterial infection -> pus consists primilariy of expended neutrophils

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22
Q

most specific antibody for SLE

A

anti-double stranded DNA

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23
Q

antibodys associated with syjogrens

A

anti Ro/La

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24
Q

antibody associated with systemic scelrosis

A

Anti-centromere

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25
Q

most specific antibodies of Rheumatoid arthritis

A

anti-citrullinated peptide antibody (CCP)

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26
Q

severe combined immunodeficiency is ?

A

dimisnished T cells / abnormal B-cells

BOTH affecteded

Xlinked or autosomal

low total lymphocyte count < 2

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27
Q

What is Burtons disease (agammaoglobuinaemia)

A

NO B-cells

Xlinked

BTK mutation in burton tyrosine gene

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28
Q

wiskott aldrish syndrome - what is it

A

X linked

b and t cell dysfunction

WASP gene mutation

(bacterial infections, eczema, thrombocytopenia - bleeding)

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29
Q

hyper-IgM syndrome

A

X linked

  • can only produce IgM

cannot differieniate

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30
Q

absence of B-cells

A

burtons (agammaglobulinaeamia)

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31
Q

selective IgA deficiency is associated with

A

coeliac disease

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32
Q

hyper IgM syndrome

A

X-linked

can only produce IgM

failure to deferientiate

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33
Q

wiskott aldrish syndrome

A

X linked

low B and T cells

  1. infection
  2. ecemza
  3. bleeding
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34
Q

most common primary immunodeficiency

A

common variable immunodeficiency

35
Q

causes of decreased antibody production

A

malnutrition

drugs

malignancy

infection

36
Q

causes of antibody loss

A

nephrotic syndromes

burns

protein losing enteropathy

37
Q

features of thalassaemia

A

jaundice, splenomegaly

poor growth and development

38
Q

pathophysiology of sickle cell

A

Autosomal recessive condition causing mutation on HBB gene on chromosome 11,

forming HbS

Results in crescent shaped RBCs, which are more prone to destruction & can block vessels

39
Q

diagnosis of sickle cell

A

New born screening @ 5 days

Definitive diagnosis is by haemoglobin electrophoresis

40
Q

management of sickle cell

A

Hydroxycarbamide – increases HbF production
Pneumococcal vaccine every 5 years

41
Q

painful sickle cell crisis

A

Obstruction of vessels by sickle cells

Triggered by dehydration, infection and deoxygenation (high altitude)

42
Q

acute chest syndrome

A

Dysponea, chest pain, low PO2,

pulmonary infiltrates on CXR

Emergency – hydration, antibiotics, resp support and analgesia

43
Q

aplastic crisis in sickle cell

A

Sudden drop in haemoglobin

Can be triggered by parvovirus B19

Supportive management, transfusion may be required

44
Q

how is haemophilia inherited

A

X linked recessive disorder
A – VIII, B – IX

45
Q

presentation of haemophilia

A

problem with clotting factors - secondary haemostasis

  • Hemarthrosis (bleeding into joints - swollen knee)
  • Intracranial bleeds, cord bleeding
  • Prolonged bleeding
46
Q

what is passive immunity

A

where a person receives pre-formed antibodies rather than producing them through their own immune system. This provides immediate but temporary protection against infections.

  1. natural - from mother
  2. injection of antibodies
47
Q

what is natural passive immunity

A

**Transfer of antibodies from mother to baby
**
- Placental IgG transfer during pregnancy

  • Breast milk (IgA)

takes Weeks to months (until antibodies degrade)

48
Q

what is artifical passive immunity

A

**Artificial Passive Immunity Injection of antibodies -
**
- Antitoxins (e.g., tetanus, diphtheria antitoxin)

  • Monoclonal antibodies (e.g., COVID-19 treatment,
    RSV prevention)
  • Immune globulin therapy (e.g., Rabies, Hepatitis B immunoglobulin)

Short-lived (few weeks to months)

49
Q

characteristics of passive immunity

A

✔ Immediate protection – Useful in emergency infections.
✔ No memory response – Does not activate the recipient’s immune system.
✔ Temporary – Antibodies degrade over time, requiring repeated administration if needed.

50
Q

What molecule trigger type 1 hypersensitivity reactions?

51
Q

what is active immunity

A

Immunity produced by the body in response to infection or vaccination.

The body produces its own antibodies.

52
Q

active immunity results in creation of memory cells

a. true
b. false

A

a. true

Yes, the body creates memory cells that remember the pathogen and respond faster upon re-exposure.

helps in long-term protection.

53
Q

speed of response in active immunity

A

Slower, as the body needs time to recognize and fight off pathogens and produce antibodies.

54
Q

key difference in active/passive immunity

A

Active immunity is the body’s natural or vaccine-induced response that creates lasting protection and memory.

Passive immunity is short-term and doesn’t involve the body’s immune system creating its own response; it relies on receiving ready-made antibodies from an external source.

55
Q

origin of b-cells and where mature

A

bone marrow

56
Q

function of b-cells

A

humerol immunity = produce antibodies

57
Q

what activates b-cells

A

antigens or Th cells (t-helper)

58
Q

b-cells and t-cells can form memory cells

59
Q

types of B cells

A

plasma cells

memory cells

60
Q

b cells interact with MHC

a. true
b. false

61
Q

function of t-cells

A

Cell-mediated immunity (kill infected cells, help B cells)

62
Q

how are t- cells activated

A

APCs antigen presenting cells

63
Q

do t-cells have memory cells

64
Q

types of t-cells

A

helper t cells

cytotoxic

regulartoy

65
Q

do t-cells interact with MHC

A

yes

both class I and II

66
Q

response time of innate immune system

A

Immediate (minutes to hours)

67
Q

response time of adpative immune system

A

Delayed (days to weeks)

68
Q

specity of innate immune system

A

Non-specific, recognizes general patterns (e.g., PAMPs)

69
Q

specificity of adapative immune system

A

Highly specific to individual pathogens

70
Q

memory of innate immune system v adapative

A

innate- - No memory (response is the same each time)

adaptive - Has memory (faster and stronger response upon re-exposure)

71
Q

components of innate immune system

A

Physical barriers (skin, mucous membranes), phagocytes, NK cells, complement system

72
Q

components of adaptive immune system

A

T cells, B cells, antibodies, antigen-presenting cells

73
Q

how is the innate system activated

A

Triggered by pathogen-associated molecular patterns (PAMPs)

74
Q

how does the innate system respond

A

Inflammatory response, phagocytosis, complement activation

75
Q

speed of activation of adapative immune system

A

Slower, requires time for activation and differentiation

76
Q

main cells in innate immune system

A

Neutrophils, macrophages, dendritic cells, NK cells

77
Q

First line of defense, prevents spread of pathogens

A

innate immne system

78
Q

Phagocytosis, inflammation, complement system

A

innate immune system

79
Q

Antibody production, cell-mediated cytotoxicity

A

adaptive immune system

80
Q

response time T4 reactions

A

48-72 hours

81
Q

response time of T2 and T3 reactions

A

hours to days

varies

82
Q

response time of T1 reactions

83
Q

mediators of T4 reactions

A

T cells (CD4 and CD8)

T cells cause tissue damage through inflammation

84
Q

Immune complexes deposit in tissues, causing inflammation
is what hypersensitivity?

A

T3

IgG nd IgM complexes with antigen

SLE/RA

85
Q

Antibodies target cells, causing destruction

is what reaction

A

T2

Haemolyic anaemia

good pastures - anti-GBM

IgM and IgG target self-cells