Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 3 Semester 2 > Immunology/Microbiology > Flashcards

Immunology/Microbiology Flashcards

1
Q

Which immune cells are polymorphonucleocytes?

A
  1. Neutrophils 2. Eosinophils 3. Basophils (granulocytes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does the tetanus vaccination work?

A

Stimulates antitoxin production

Does not prevent the growth of C. tetani in wounds, but protects against the toxin produced by the organism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Which tetanus vaccination is given to children?

A

DTPa

(diphtheria, tetanus, pertussis (acellular))

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which tetanus vaccination is given to adolescents and adults?

A

dTpa

Contain substantially less amounts of diphtheria toxoid and pertussis antigens than DTPa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

When should adults receive a tetanus booster dose?

A

All adults aged 50 who have not had a tetanus booster in the previous 10 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

When is tetanus immunoglobulin (TIG) given?

A

If there is any doubt about the adequacy of previous tetanus immunisation in a person with a tetanus-prone wound

e.g. immunodeficiency, <3 tetanus doses or uncertain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which organism causes tetanus?

A

Clostridium tetani

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which cells are phagocytes?

A
  1. Monocytes (macrophages, dendritic cells)
  2. Mast cells
  3. Neutrophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the action of C5a?

A

Chemotaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the action of C3b?

A

Opsonisation (with the action of C5a)

+ helps create MAC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which complement proteins are involved in the formation of the MAC?

A

C5b, C6, C7, C8, C9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which complement pathway requires the adaptive response for activation?

A

Classical

Activated by antigen-antibody complexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are anaphylatoxins?

A

Bind to and stimulate mast cells and basophils to degranulate

Complement peptides C3a, C4a and C5a

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which T helper cells are involved in autoimmune reactions?

A

Th1 or Th17

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which T helper cells are involved in allergic reactions?

A

Th2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are 3 organisms people with asplenism particularly susceptible to?

A

Streptococcus pneumonia

Neisseria meningitidis

Haemophilis influenzae

Klebsiella

Pseudomonas aureginosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

In which area of the spleen are APCs and specialised B cells found?

A

Marginal zone

Between the red and white pulp - area where APCs present blood-bourne antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

In which area of the spleen are T cells found?

A

Periarterial lymphatic sheath of the white pulp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Which immunoglobulins are measured when investigating immunodeficiency?

A

IgA, IgG, IgM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are 3 congenital B-cell immunodeficiencies?

A

Brunton agammaglobulinemia (X-lined agammaglobulinemia)

Selective IgA deficiency (SIgAD)

Common variable immunodeficiency (CVID)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

In which immunodeficiency are B cells phenotypically normal but unable to differentiate into Ig-producing cells

A

Common variable immunodeficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the most common congenital immunodeficiency?

A

Selective IgA deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Which congenital B cell immunodeficiency typically has an onset at 20-35 years of age?

A

Common variable immunodeficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What type of infections are characteristic of complement deficiencies?

A

Infections from encapsulated organisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What type of infections are characteristic of granulocyte deficiencies?

A

Skin and soft tissue infections

Catalase-positive organisms e.g. Staph aureus, Gram -ve bacilli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What type of infections are characteristic of T cell deficiencies?

A

“Benign” viruses (e.g. CMV, EBV), fungi, intracellular pathogens (e.g. mycobacteria)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the function of PRR and PAMPs?

A

Pattern recognition receptors (PRRs) recognise pathogen-associated molecular patterns (PAMPs) and induce cytokine release

PAMPs = products found in pathogens and not in mammals e.g. flagellin

PRR e.g. toll-like receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the common end point of the three complement pathways?

A

Splitting of C3 into C3a and C3b

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the function of C3a

A

Histamine degranulation → enhanced inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is a bacterial capsule?

A

Polysaccharide layer that lies outside the cell envelope

Prevents phagocytosis

A capsule-specific antibody is required

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the structure of immunoglobulins?

A

Two heavy chains

Two light chains

The variable regions of the H and L chains are the antibody binding sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Which immunoglobulin crosses the placenta and provides passive immunity to children?

A

IgG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Which immunoglobulin is least affected by loss of immunoglobulins in the renal or gastrointestinal tract?

A

IgM

Largest of the immunoglobulins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Which is the most potent cytokine?

A

IL-6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

How do glucocorticoids suppress the immune system?

A

Decreased transcription of pro-inflammatory genes

→ Inhibits neutrophil binding to the vessel wall (less emigration to tissues)

→ Inhibits leukocyte activity

  • Neutrophil infections - staph, strep, candida*
  • Lymphocyte infections - herpes, mycobacteria, salmonella*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Delayed loss of the umbilical cord is associated with which immunodeficiency?

A

Leukocyte adhesion deficiency

Poor migration of immune cells from the vessel wall, particularly neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is defective in chronic granulomatous disease?

A

Deficiency of superoxide production by polymorphoneutrophils and macrophages → ability to ingest but not kill microorganisms → granuloma formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the mechanism of natalizumab?

A

Stops leukocytes from adhering to vessel walls

Cannot reach tissues to cause inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the mechanism of fingolimod?

A

Blocks sphingosine-1-phosphate receptor

Lymphocytes accumulate in lymph nodes → not able to travel to tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

When is infection a contraindication to vaccination?

A

Temperature > 38.5 degrees

Minor coughs and colds are ok

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Which test is used to assess the complement system?

A

CH100/50

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How do immunomodulators affect infection risk?

A

They do not increase the risk of infection as they are not immunosuppressive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the mechanism of azathioprine?

A

Purine antimetabolite

Impairs lymphocyte proliferation, cellular immunity and antibody responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What feature is unique to splenic macrophages?

A

Can detect and capture encapsulated bacteria

Normal macrophages detect proteins, but the polysaccharide wall is a sugar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is a unique feature of B cells in the splenic marginal zone?

A

Can initiate T cell-independent immune reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What occurs in the cortex of lymph nodes?

A

B cell proliferation occurs in germinal centres

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What lies in the paracortex of lymph nodes?

A

T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is the role of dendritic cells in lymph nodes?

A

Dendritic cells are activated → enter lymph node → present antigen to T cells → T cells activate B cells → antibody production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Why are patients with diabetes immunocompromised?

A

Neutrophil dysfunction → bacterial and fungal infections

Poor peripheral circulation → ulceration + poor delivery of neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Which immunoglobulin(s) are affected by asplenism?

A

IgM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Which immunoglobulin is involved in type III hypersensitivity reactions?

A

IgG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Why do type I hypersensitivity reactions occur so rapidly?

A

IgE coats mast cells and basophils with initial contact with the antigen

Antigen readily binds to IgE with subsequent exposure and causes degranulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Which immunoglobulin(s) are involved in type II hypersensitivity reactions?

A

IgM and IgG

Bind to antigens → complement activation → cellular lysis and phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is tryptase?

A

Specific marker of mast cell activation

If elevated → increased risk of anaphylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is the mechanism of montelukast?

A

Leukotriene receptor antagonist

May be used for long-term asthma control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is the mechanism of complement-dependent type II hypersensitivity reactions?

A
  1. IgG and IgM bind to antigens
  2. Complement activation (classical)
  3. Cellular lysis or phagocytosis
    * E.g. autoimmune haemolytic anaemia, pemphigus vulgaris, drug reactions*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is the mechanism of antibody-dependent cell-mediated cytotoxic type II hypersensitivity reactions?

A

Ab + Ag → activation of NK cells → cell lysis without phagocytosis

Destruction of targets too large to be phagocytosed e.g. parasites, tumour cells, graft rejection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is the mechanism of antibody-mediated cellular dysfunction type II hypersensitivity reactions?

A

Antibodies directed against cell surface receptors → impaired or dysregulated cell dysfunction

E.g. MG, Goodpasture’s, pernicious anaemia, acute rheumatic fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What type of hypersensitivity is myasthenia gravis?

A

Type II (antibody-mediated cellular dysfunction)

Antibodies bind to post-synaptic ACh receptors, competing with ACh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What type of hypersensitivity reaction is Goodpasture’s syndrome?

A

Type II (antibody-mediated cellular dysfunction)

Antibodies against type IV collagen (in basement membrane of glomerulus → glomerulonephritis + acute renal failure)

Can also affect alveoli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What type of hypersensitivity reaction is pernicious anaemia?

A

Type II (antibody-mediated cellular dysfunction)

Antibodies against intrinsic factor and/or parietal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What type of hypersensitivity reaction is autoimmune haemolytic anaemia and acute haemolytic transfusion reaction?

A

Type II (complement-dependent)

63
Q

What type of hypersensitivity reaction is pemphigus vulgaris?

A

Type II (complement-dependent)

64
Q

What type of hypersensitivity reaction is rheumatic fever?

A

Type II

Antibodies against streptococcal M protein

65
Q

What type of hypersensitivity reaction is lupus?

A

III

66
Q

What are the two forms of type IV hypersensitivity?

A
  1. Delayed-type
  2. T-cell mediated
67
Q

What is the pathophysiology of delayed-type IV sensitivity?

A

Antigen exposure → CD4+ and MHC-II activation → CD4+ differentiation to TH1 → inflammatory reaction

E.g. TB skin test, contact dermatitis, granulomatous inflammation

68
Q

What is the pathophysiology of cell-mediated cytotoxic IV sensitivity?

A

Sensitisation of CD8+ cells

Graft rejection, viruses, tumour immunity, intracellular pathogens e.g. TB

69
Q

What type of hypersensitivity reaction is GBS?

A

Type IV

70
Q

What type of hypersensitivity reaction is T1DM?

A

Type IV

71
Q

What is the role of glucocorticoids in anaphylaxis?

A

Prevention of late phase reaction (limited evidence, but no harm)

72
Q

What are 3 mechanisms of peripheral T cell tolerance?

A
  1. Anergy (no second signal)
  2. Block in activation (suppression)
  3. Deletion (apoptosis)
73
Q

What types of vaccination are given to asplenic patients?

A

Conjugate or recombinant

Both contain have a protein component which stimulates T cell proliferation

74
Q

Which type of bones contain red bone marrow?

A

Flat bones e.g. pelvis

Long bones

75
Q

What is positive selection?

A

T cells that generate a functional receptor and can bind with self MHC molecules proliferate

76
Q

What is negative selection?

A

Removes thymocytes that bind to MHC self-peptides

77
Q

What is the most common cause of angioedema from direct mast-cell activation (non-IgE mediated)?

A

NSAIDs

78
Q

What is the risk of HIV transmission in MSM?

A

0.5% for a receptive partner

79
Q

What is the risk of HIV transmission in male to female intercourse?

A
  1. 1% for female partner
  2. 05% for male partner
    * HIV concentration is higher in male ejaculate than in vaginal secretions*
80
Q

Which HIV proteins help the virus attach to CD4 receptors?

A

gp120 and gp41 (envelope proteins)

81
Q

Which protein helps viruses convert viral RNA to DNA?

A

Reverse transcriptase

82
Q

Which protein is required to insert viral genes into the host genome?

A

Integrase

83
Q

What is the definition of a retrovirus?

A

Genome is stored in RNA rather than DNA

84
Q

Which immune cells have CD4 receptors?

A

T lymphocytes

Macrophages

Monocytes

Dendritic cells

85
Q

Which two things must be present for HIV virus to enter a cell?

A

CD4 receptor

Coreceptor (CCR4 in T cells and CCR5 in all other CD4 cells)

86
Q

A mutation in what is associated with HIV immunity?

A

Homozygous CCR5 mutation = immunity

Heterozygous CCR5 mutation = slower disease progression due to impaired viral spread

87
Q

What is acute retroviral syndrome?

A

Acute HIV syndrome

Fever, fatigue, lymphadenopathy, myalgia/arthralgia, headache, rash, GI symptoms, sore throat, ulcerations, painful swallowing

Similar to mono (rashes and diarrhoea more prevalent)

88
Q

What is HIV wasting syndrome?

A

Unintentional weight loss of >10%, fever, fatigue, diarrhoea

89
Q

What is kaposi sarcoma?

A

Tumour of the skin and mucosa caused by herpes virus 8

Most common HIV-associated tumour

90
Q

What is the most common opportunistic bacterial infection in AIDS patients?

A

Mycobacterium avium complex (MAC infection)

91
Q

What is progressive multifocal leukoencephalopathy?

A

Reactivation of JC virus → infects oligodendrocytes → aggressive replication within brain tissue → destruction of infected oligodendrocytes + demyelination

Focal symptoms, seizures, impaired vigilance, cognitive disorders, behavioural changes

92
Q

What is the most common cause of death in AIDS patients?

A

Pneumocystitis pneumonia

  • Caused by pneumocystitis jiroveci (fungus)*
  • Occurs almost exclusively in immunocompromised patients*
93
Q

What is the HIV window period?

A

Time between infection and detectability of HIV antibodies

2-6 weeks

94
Q

List 10 AIDS-defining conditions

A
  1. HIV wasting syndrome
  2. Kaposi sarcoma
  3. Invasive cervical cancer
  4. Lymphoma (non-Hodgkin)
  5. TB reactivation
  6. Coccidioidomycosis
  7. Cryptosporidiosis
  8. HIV-related encephalopathy (AIDS dementia)
  9. PML
  10. Pneumocystitis pneumonia
  11. Isosporiasis
  12. Histoplasmosis
  13. Cerebral toxoplasmosis
  14. Cryptococcosis
  15. Candidiasis
  16. Herpes simplex infections
  17. CMV infection (other than spleen, lymph nodes or liver)
  18. MAC infection
95
Q

A CD4 count less than what is definitive of AIDS irrespective of symptoms?

A

<200 cells/uL

96
Q

Which virus causes Kaposi sarcoma?

A

Herpes virus 8

97
Q

What is the first-line investigation for diagnosing HIV?

A

HIV Ag/Ab

  • Detects HIV antigen (p24) and anti-HIV antibodies*
  • Near 100% sensitivity*
98
Q

Which allele should be tested upon initiation of abacavir?

A

HLA-B*5701

Hypersensitivity

99
Q

What are 4 drug classes used in the treatment of HIV?

A
  1. Nucleoside reverse transcriptase inhibitors
  2. Non-nucleoside reverse transcriptase inhibitors
  3. Protease inhibitors
  4. Integrase inhibitors
  5. Fusion inhibitor
  6. Nucleoside analogues
  7. CCR5-antagonist
100
Q

What is the most common HIV retroviral regimen?

A

2 NRTI + 1 NNRTI / protease inhibitor / integrase inhibitor

101
Q

Name 4 first-line nucleoside reverse transcriptase inhibitors

A
  1. Tenofovir
  2. Emtricitabine
  3. Abacavir
  4. Lamivudine
    * 5. Zidovudine*
    * 6. Stavudine*
    * 7. Didanosine*
    * mostly end in “-ine”*
102
Q

What is the first-line non-nucleoside reverse transcriptase inhibitor?

A

Efavirenz

Other: Nevirapine

103
Q

Name two first-line protease inhibitors

A
  1. Atazanavir
  2. Darunavir
    * Indinavir*
    * Ritonavir*
    * Nelfinavir*
    * Lopinavir*
    * end in “-avir”*
104
Q

Name two integrase inhibitors

A

Raltegravir

Dolutegravir

end in “-gravir”

105
Q

What are 3 adverse effects of nucleoside reverse transcriptase inhibitors?

A
  1. Bone marrow suppression (neutropenia, anaemia)
  2. Mitochondrial toxicity (lactic acidosis, myopathy, neuropathy)

3. HIV-associated lipodystrophy

  1. Hypersensitivity (abacavir)
  2. Pancreatitis (didanosine/stavudine)
106
Q

—– is a CNS protozoal infection that presents with brain abscesses in HIV patients, that are seen as ring-enhancing brain lesions on CT/MRI

A

Toxoplasmosis

107
Q

Which protozoa causes toxoplasmosis?

A

Toxoplasma gondii

108
Q

How is toxoplasmosis transmitted?

A

The oocytes are excreted in the faeces of cats and are orally ingested by other mammals such as humans, hoofed animals, and birds. Primary modes of transmission therefore include:

Cat feces

Raw or insufficiently cooked meat

Unpasteurized milk (especially goat milk)

109
Q

Which opportunistic fungus causes pneumonia in HIV patients?

A

Pneumocystic jirovecii

110
Q

Which type of vaccination should not be given to immunocompromised patients?

A

Live attenuated

111
Q

—— is a dermatological infection caused by EBV in HIV patients that commonly presents on the lateral tongue

A

Hairy leukoplakia

112
Q

—— is a protozoa that causes GI infection in HIV patients that presents with chronic, watery diarrhoea

A

Cryptosporidium spp

Acid fast cysts are seen in the stool

113
Q

——- is an opportunistic fungus that causes meningitis in HIV patients

A

Cryptococcus neoformans

114
Q

Which immune cells can a monocyte differentiate into?

A
  1. Macrophage
  2. Dendritic cells
  3. Microglial cell
    * Monocyte in blood, other cells in tissue*
115
Q

When is HIV transmission greatest?

A

Acute infection

Viral load is high

116
Q

Which 4 features are most discriminatory between acute HIV infection and EBV?

A
  1. Profound malaise
  2. High fever
  3. Weight loss
  4. Mouth ulcers
117
Q

How is oral candida distinguished from hairy cell leukoplakia?

A

Oral candida is not adherent and can be removed with scratching

Leukoplakia is more adherent

118
Q

Which organism causes hairy cell leukoplakia?

A

EBV

119
Q

Candidiasis involving which organs is an AIDS-defining illness?

A

Bronchi, trachea, lungs, or oesophagus

120
Q

Retinitis of which pathogen is an AIDS-defining illness?

A

CMV retinitis

121
Q

Primary CNS lymphoma is an AIDS-defining illness associated with which infection?

A

EBV

122
Q

What prophylaxis is given to HIV patients for pneumocystis pneumonia and when?

A

Trimethoprim-sulfamethoxazole

CD4 < 200 cells/mm3

123
Q

What prophylaxis is given to HIV patients for toxoplasma gondii and when?

A

Trimethoprim-sulfamethoxazole

CD4 < 100 cells/mm3

124
Q

What prophylaxis is given to HIV patients for TB and when?

A

Isoniazid + pyridoxine

Positive tuberculin skin test or interferon-gamma release assay (i.e. latent)

125
Q

What prophylaxis is given to HIV patients for MAC disease and when?

A

Azithromycin or clarithromycin

CD4 <50

126
Q

Why is the majority of CD4+ death in HIV from non-infected cells?

A
  1. HIV attracts T cells to lymph nodes
  2. HIV virus releases an interleukin which promotes intracellular inflammation in T cells
  3. T cells undergo PYROPTOSIS
  4. Debris from pyroptosis induces inflammation in surrounding T cells
  5. Cascade of pyroptosis and inflammation
127
Q

Name 5 non-AIDS HIV syndromes

A
  1. Immune thrombocytopaenia purpura
  2. GBS
  3. Bell’s palsy
  4. Psoriasis
  5. Seborrheic dermatitis
  6. Oral hairy leukoplakia
  7. Oral candida
  8. HSV
  9. HZV
  10. Gingivitis
  11. Molluscum contagiosum
128
Q

What adverse effect(s) are associated with tenofovir?

A

Nephrotoxicity

Osteoporosis

129
Q

What adverse effect is associated with efavirenz (NNRTI)?

A

CNS toxicity (give before bed)

130
Q

What adverse effect(s) are associated with atazanavir (PI)?

A

Jaundice

Renal stones

131
Q

What adverse effect is associated with integrase inhibitors?

A

Myositis

132
Q

What is a toxicoid vaccine?

A

Stimulates immunity to toxins, not to the organism itself

Vaccine contains toxoids (inactivated toxins)

e.g. tetanus, diptheria

133
Q

What is a subunit vaccination?

A

Vaccine presents an antigen to the immune system without introducing the pathogen

Includes toxoid, polysaccharide, conjugate and recombinant vaccines

134
Q

What is a conjugate vaccine?

A

Polysaccharide from encapsulated bacteria + carrier protein

B cell responses to capsular polysaccharides are T cell indepednent

By conjugating the polysaccharide to a protein carrier, a T cell response can be induced

T cells stimulate a more vigorous immune response and have more rapid, long-lasting immunologic memory

135
Q

What is a recombinant vaccine?

A

Genes that encode antibody formation are inserted into the DNA of other cells e.g. yeast

When this harmless cell replicates in the body, antibody production occurs

E.g. hepatitis B, HPV

136
Q

What is a polysaccharide vaccine?

A

Contains part of the polysaccharide shell of encapsulated bacteria

E.g. Pneumovax (Streptococcus pneumoniae)

137
Q

What is the function of protease?

A

Cleavage of viral proteins into functional polypeptides (core proteins)

These proteins then form the viral capsid

138
Q

What is an arthus reaction?

A

Antibody/antigen complex formation in the skin –> local inflammation +/- necrosis (type III hypersensitivity)

Most commonly following booster vaccinations

More likely if boosters are given close together and circulating antibodies are high

139
Q

How are B cells activated?

A
  1. Antigen is presented to B cells
  2. B cells express antigen on MHC-II
  3. Helper T cells provide costimulation
140
Q

What constitutes a complete tetanus immunisation schedule?

A

3 primary (2, 4 and 6 months of age)

+ 2 booster (ideally 18 months and 4 years)

141
Q

A person in ARV therapy for HIV develops jaundice and renal stones

Which drug is likely to have caused these effects?

A

Atazanavir

142
Q

A person in ARV therapy for HIV develops myositis

Which drug is likely to have caused these effects?

A

Raltegravir

Dolutegravir

143
Q

Which medications are in TRUVADA (for PrEP)?

A

Emtricitabine and tenofovir

144
Q

Why do patients with CVID have low immunoglobulin levels?

A

B cell dysfunction and poor differentiation → impaired antibody production

145
Q

What type of infections are most common in patients with B cell immunodeficiencies?

A

Sinopulmonary (pneumonia, bronchitis, sinusitis, otitis, conjunctivitis)

Chronic diarrhoea (norovirus, campylobacter jejuni, salmonella)

146
Q

What is the difference between humoral and cellular immunity?

A

Humoral = antibody-mediated. Acts on extracellular microbes

Cellular = T cells, NK cells, macrophages. Acts on intracellular microbes

147
Q

What is the pathophysiology of allergic contact dermatitis?

A
  1. Allergen enters the dermis and is picked up by a dendritic cell
  2. Allergen is presented on MHC-II
  3. T helper cells recognises antigen and binds to MHC-II with CD4 coreceptor
  4. Dendritic cell releases IL-12, stimulating maturation and differentiation of the CD4 cell to a Th1 cell
  5. Th1 cell releases inflammatory mediators

Repeated contact with allergen stimulates memory T cells

148
Q

What is the pathophysiology of urticaria?

A
  1. Allergen is picked up and presented in lymph nodes by APCs
  2. CD4 cell binds to APC and differentiates into a Th2 cell
  3. Th2 cell stimulates class switching of B cells, so IgE (not IgM) is produced
  4. IgE binds mast cells (sensitisation)
  5. Mast cell activation → inflammatory reaction
  6. Subsequent exposure to allergen → quick reaction due to preformed IgE
149
Q

When is the onset of x-linked agammaglobulinemia?

A

>4 months after birth

150
Q

What is defective in x-linked agammaglobulinemia?

A

Complete B cell deficiency

151
Q

Which non-infectious conditions are associated with selective IgA deficiency?

A

Coeliac

IBD

152
Q

Which non-infectious conditions are associated with CVID?

A

Lymphoma, gastric cancer

Autoimmune disorders e.g. RA, autoimmune haemolytic anaemia, immune thrombocytopenia, vitiligo

153
Q

What is the RAST?

A

Radioallergosorbent test

Detects specific IgE antibodies

Year 3 Semester 2 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions