Brainscape's Knowledge GenomeTM

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


See full index

Dermatology > Immunology > Flashcards

Immunology Flashcards

You may prefer our related Brainscape-certified flashcards:
Dermatology Board Prep flashcards
1
Q

how is the keratin layer formed?

A

through terminal differentiation of keratinocytes to corneocytes

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

name some important structural proteins in the keratin layer & epidermis

A

filaggrin
involucrin
keratin

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

name some features of the keratin layer

A

tough
lipid rich
physical barrier

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

what do keratinocytes do in the epidermis?

A

sense pathogens via cell surface receptors and help mediate an immune response

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

what can keratinocytes be activated in the epidermis?

A

UV light

sensitzers e.g. allergic contact dermatitis

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

what do keratinocytes produce in response to pathogens?

A

antimicrobial peptides (AMPs)
cytokines
chemokines

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

what are Langerhans cells?

A

a type of dendritic cell that intersperse with keratinocytes in the epidermis

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

what are Langerhans cells characterised by?

A

the birbeck granule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what do Langerhans cells do?

A

process lipid Ag & microbial fragments & present them to effector T cells to activate them

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

what type of T cells are found in the skin?

A

mainly CD8+ in the epidermis
CD4+ & CD8+ in the dermis
subsets (NK cells) are also found

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

which CD4+ Th cells are associate with inflammation?

A

Th1 - psoriasis
Th2 - atopic dermatitis
Th17 - atopic dermatitis & psoraisis

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

where are T cells produced?

A

bone marrow

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

where are T cells sensitised?

A

thymus

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

how are Ags recognised and T cells activated?

A

using the T cell receptor (TCr) & major histocompatibility complex (MHC)
enhanced by co-recptors

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

what do Th1 cells do?

A

activate macrophges to destroy macrophages using IL2 & IFN gamma

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

when are Th1 cells especially useful?

A

against viral invaders

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

what do Th2 cells to?

A

help B cells to make Ab using IL4, IL5 & IL6

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

when are Th2 cells especially useful?

A

against parasitic invaders

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

when are CD8+ cells useful?

A

important in the protection against viruses & cancer

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

which types of dendritic cell are found in the dermis?

A

dermal dendritic cell & plasmacytoid dendritic cell

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

what do dermal DCs do?

A

involved in Ag presenting & secreting cytokines & chemokines

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

what do plasmacytoid DCs do?

A

produce IFN alpha

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

when are plasmacytoid DCs found in the skin?

A

they are low or absent in normal skin but found in relatively high numbers in diseased skin

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

what is psoriasis?

A

an over-reaction of the immune response presenting as chronic inflammation, specifically a non-late phase wound response

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

describe the immunopathogeneis of psorasis

A

keratinocytes under stress release factors that stimulate pDC to produce IFN alpha, interleukins& TNF which activate DC which migrate to lymph nodes to present to & activate Th cells
T cells then attracted to dermis by cheekiness & secrete interleukins

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

what is the key factor in atopic eczema?

A

impairment of the skin barrier function due to mutations in the filaggrin gene and decreased AMP in skin

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

how does impairment of the skin barrier function cause atopic eczema?

A

allows access/sensitisation to allergen & promotes colonisation by micro-organisms

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

what does filaggrin do in normal skin?

A

normally found in granules in granular layer where it breaks down & binds water helping the skin to retain water, naturally moisturising the skin

29
Q

which interleukin is clinically relevant in eczema?

A

IL4

30
Q

what happens in vitiligo?

A

melanocytes are attacked by T lymphocytes

31
Q

what happens in SLE?

A

auto-antibodies are produced by B lymphocytes

32
Q

when are Type II hypersensitivity mechanisms important?

A

in autoimmunity & transplantation

mediated by IgG & IgM

33
Q

when are type III hypersensitivity mechanisms important?

A

in certain drug reactions

mediated by IgG & IgM

34
Q

when are type i hypersensitivity mechanisms important?

A

in allergies

mediated by IgE

35
Q

when are type IV hypersensitivity mechanisms important?

A

in contact allergies & tuberculin reaction

mediated by Th1 cells

36
Q

which factors affect skin immune response in organ transplant?

A

immunosuppression - after 10 years most probable cause of death is skin cancer as its more like to metastasis due to lack of active immune surveillance

37
Q

which factors affect skin immune response to UV light?

A

immunosuppression & structure

38
Q

which factors affect skin immune response in ageing?

A

changes in skin structure
decreased ability to detect maligned cells
decreased ability to detect Ag
decreased ability to distinguish self cells from non-self

39
Q

what 2 types of drug reactions are there?

A

immunologically mediated reactions & non-immunologically mediated reactions

40
Q

what types of immunologically mediated drug reactions are there?

A

type 1 - anaphylactic
type 2 - cytotoxic reactions
type 3 - immune complex-mediated reactions
type 4 - cell mediated delayed hypersensitivity reactions

41
Q

are immunologically mediated drug reactions does dependant?

A

no

42
Q

what non-immunologically mediated drug reactions are there?

A 
eczema
drug induced alopecia
phototoxicity 
skin erosion/atrophy from topical therapy 
psoraisis 
pigmentation
43
Q

are non-immunologically mediated drug reactions does dependant?

A

can be

44
Q

who do drug reactions present?

A 
exanthematous/morbiliform/maculopapular 
urticarial 
papulosquamous/pustular/bullous 
pigmentation 
itch/pain 
photosensitivity
45
Q

what are the risk factors for developing a drug eruption?

A 
age - young adults > infants/elderly
gender - females > males
genetics 
concomitant disease 
immune status
chemistry 
route 
does 
kinetics/half-life
46
Q

what are exanthematous drug eruptions?

A

Most common type of drug eruption (90%).

Idiosyncratic, T-cell mediated delayed type hypersensitivity (Type IV) reaction,

47
Q

describe some of the clinical features of an exanthematous drug eruption

A

usually mild & self-limiting
widespread symmetrically distributed rash sparing the mucous membranes
pruritus & mild fever is commone

48
Q

what are the indicators of a potential severe reaction in exanthematous drug eruptions?

A 
Involvement of mucous membrane and face.
Facial oedema & erythema.
Widespread confluent erythema.
Fever (>38.5⁰C).
Blisters, purpura, necrosis.
Lymphadenopathy, arthalgia.
Shortness of breath, wheezing.
49
Q

name some drugs associated with exanthematous drug eruptions (at least 4)

A 
Penicillins
Sulphonamide antibiotics
Erythromycin
Streptomycin
Allopurinol
Anti-epileptics: carbamazepine
NSAIDs
Phenytoin
Chloramphenicol
50
Q

what is the mechanism of urticarial drug reactions?

A

IgE mediated hypersensitivty reaction after rechallenge with drug or direct release of inflammatory mediators from mast cells on first exposure

51
Q

give 2 examples of pustular/bullous drug eruptions

A

acne

acute generalised exanthematous pustulosis (AGEP)

52
Q

what do fixed drug eruptions look like?

A

well demarcated round/ovoid plaques

53
Q

what do fixed drug eruptions feel like?

A

red & painful

54
Q

where are fixed drug eruptions found?

A

hands, genitalia, lips & occasionally oral mucosa

55
Q

how do fixed drug eruptions resolve?

A

with persistent pigmentation when the drug is stopped

56
Q

can fixed drug eruptions re-occur?

A

yes, on the same site on re-exposure to the drug

57
Q

how fixed drug eruptions present?

A

as eczematous lesions, papules, vesicles or urticaria

58
Q

which drugs are associated with fixed drug eruptions?

A

tetracylcine, doxycycline, paracetamol, NSAIDs, carbamazepine

59
Q

what do combined cutaneous and systemic symptoms include in severe cutaneous adverse reactions?

A

stevens-johnson sydrome
toxice epidermal necrolysis
drug reaction with eosinophilia & systemic symptoms
acute generalised exanthematous pustulosis

60
Q

what is stevens-johnson syndrome (SJS)?

A

a form of toxic epidermal necrolysis, is a life-threatening skin condition, in which cell death causes the epidermis to separate from the dermis

61
Q

what is toxic epidermal necrolysis (TEN)?

A

also known as Lyell’s syndrome, is a rare, life-threatening skin condition that is usually caused by a reaction to drugs

62
Q

what is drug reaction with eosinophilia& systemic symptoms (DRESS)?

A

a severe idiosyncratic drug reaction with a long latency period

63
Q

what is acute generalised exanthematous pustulosis (AGEP)?

A

a common cutaneous reaction pattern that is characterized by a sudden eruption that appears on average five days after the medication is started

64
Q

what are the acute phytotoxic drug reactions?

A

skin toxicity
systemic toxicity
photodegradation

65
Q

what are the chronic phytotoxic drug reactions?

A

pigmentation
photoageing
photocarcinogenesis

66
Q

what are photooptic cutaneous drug reactions?

A

Non-immunological mediated skin reaction which will arise in any individual providing there is enough photo-reactive drug and the appropriate wavelength of light

67
Q

what is the waveband usually associated with phototoxic cutaneous drug reactions?

A

UVA/Visible

68
Q

what are the major patterns of cutaneous phototoxicity?

A

immediate prickling with delayed erythema & pigmentation
exaggerated sunburn
exponsed telangiectasia
delayed 3-5 days erythema & pigmentation
increased skin fragility

Dermatology (16 decks)

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