Brainscape's Knowledge GenomeTM

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


See full index

pr3152 > allergies and hypersensitivities > Flashcards

allergies and hypersensitivities Flashcards

1
Q

what is an allergy

A

immunological mediated hypersensitivity response to a substance in a sensitised person

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

what does an allergy cause

A

response of immune response to an antigenic substance leads to host tissue damage, manifesting as a organ specific or generalised systemic reaction

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

what are drug hypersensitivity reactions

A

includes adverse events that clinically resemble drug allergy but have yet proven to be associated with an immune response

drugs that can cause the release of mast cells and basophil derived mediators by a pharmacological/ physical effect rather than IgE

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

what are the effectors of allergic/ drug hypersensitivity reactions

A

major components of innate and adaptive immunity, pharmacologically active chemical mediators

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

what are the components of innate and adaptive immunity

A

cellular components, complements, cytokines, Ig

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

what are examples of pharmacologically active chemical mediators

A

histamine, platelet aggravating factors, thromboxanes, prostaglandins, leukotrienes

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

what are granulocytes

A

type of WBC that degranulates and release whole bunch of toxic substances that can damage both invading and nearby host cells

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

what is type 1 hypersensitivity

A

IgE mediated, occurs within minutes, genetic predisposition that makes T cells mores sensitive to allergen

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

what is the process of type 1 hypersensitivity

A

sensitisation phase: T cells bind to specific molecule on allergen and present it to APC which mounts an immune response if allergic, after this the naive T cells become primed and are now Th2 cells, when excited, it releases IL4 which causes B cells to undergo class switching and produce IgE Ab instead of IgM and will also release IL5 which stimulate production and activation of eosinophils. since IgE are highly specific they bind to Fce receptor on mast cells

early phase response: mast cells now have Fce receptor and IgE which will bind to allergen during reexposure causing degranulation of mast cell and thus release of mediators and cause effects of allergic reaction

late phase response: recruitment of more immune cells to site of allergen due to cytokines and mediators released

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

what are the mechanisms of injury in a type 1 hypersensitivity reaction

A

mast cell derived mediators and cytokine derived inflammation

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

what are examples of mast cell derived mediators

A

vasoactive amines, lipid mediators, cytokines

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

what are examples of cytokines that cause inflammation

A

eosinophils and neutrophils

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

what are the components involved in type 1 hypersensitivity

A

Th2 cells, eosinophils, IgE, mast cells

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

what is type 2 hypersensitivity

A

antibody mediated hypersensitivity, cytotoxic hypersensitivity, occurs due to escaped self reactive T and B cells which causes autoimmune disease if target healthy cells

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

what is the process of type 2 hypersensitivity

A

Ag bind to RBC which causes IgG specific to Ag to bind to Ag and form Ab-Ag complex which activates the complement system to kill off RBC

mechanism 1: C1 binds to Fc of Ab -> activate C2-C9 -> some get cleaved into chemotactic factors which attracts neutrophils -> degranulate and release oxygen radicals that are highly cytotoxic -> cell death and tissue damage

mechanism 2: C5b, C6-9 come together to attack complex, MAC inserts within cell membrane, causing channels to form which allows fluid and molecules to flow into and out -> osmotic difference causes fluid to rush in -> bursting of cell (lysis)

mechanism 3: IgG bind to C3b -> cell opsonised and targeted by phagocytosis by macrophages and neutrophils by targeting Fc domain of Ab of C3b bounded to IgG -> engulf and destroy

mechanism 4: Ab-Ag complex recognised by NK cells by Fc domain of Ab -> release of toxic granules -> causes perforation -> allows not only fluid but also enzymes which causes apoptosis of cells

mechanism 5: cellular dysfunction

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

what are the mechanisms of injury in type 2 hypersensitivity

A

complement and Fc receptor mediated recruitment and activation of leukocytes, opsonisation and phagocytosis of cells, abnormalities in cellular dysfunction

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

what are the components involved in type 2 hypersensitivity

A

IgG, IgM, extracellular matrix Ag

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

what is type 3 hypersensitivity

A

immune complex mediated hypersensitivity

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

what is the process of type 3 hypersensitivity

A

Ab are produced by plasma cells, IgM attaches to Ag which is presented to T cell -> T cell releases cytokines -> B cell activation and class switching from IgM to IgG -> smaller Ab-Ag complexes get deposited on vessel walls and not engulfed by macrophages -> activate complement system -> C1 binds to complement -> C2-C9 activated -> cleaved into fragments -> attract neutrophils -> try to phagocytose but cannot so degranulate -> release lysosomal enzymes and reactive oxygen species -> inflammation

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

what are plasma cells

A

fully matured and differentiated B cells

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

what are the components involved in type 3 hypersensitivity

A

IgM/IgG -Ag complexes deposited in vascular basement membrane

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

what is type 4 hypersensitivity

A

T cell mediated diseases

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

what is the process of type 4 hypersensitivity

A

Ag presented by APC to T cell via MHC II molecule -> release cytokine

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

what are the mechanisms of injury in type 4 hypersensitivity

A

macrophage activation, cytokine mediated inflammation for CD4+

direct target cell lysis, cytokine mediated inflammation for CD8+

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

what are the components involved in type 4 hypersensitivity

A

CD4+, MHC II, CD8+, MHC I

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

what are immune complexes

A

only if Ab bind to soluble Ag flowing freely in blood, not considered if Ab bind to Ag on cell surface

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

what are the clinical manifestations of hypersensitivity reactions

A

anaphylaxis, drug fever, drug induced autoimmunity, vasculitis, respiratory, hematologic

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

what is anaphylaxis

A

acute life threatening reaction that involves multiple organ symptoms

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

what are drugs commonly associated with anaphylaxis

A

NSAIDs, penicillin, insulin

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

what is drug fever caused by

A

systemic reactions caused by circulating immune complexes

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

what are drugs commonly associated with drug fever

A

abx

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

what are drugs commonly associated with vasculitis

A

allopurinol, thiazide

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

what are drugs commonly associated with respiratory manifestations

A

asthma - NSAIDs
acute infiltrative and chronic fibrotic pulmonary reactions - bleomycin, nitrofurantoin

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

what are examples of a hematologic manifestation

A

eosinophilia, hemolytic anemia, thrombocytopenia, agranulocytosis

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

what is are the examples of SCAR

A

drug rash with eosinophilia and systemic symptoms (DRESS), mucocutaneous disorders (SJS, TEN)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what is DRESS

A

triad of rash, eosinophilia and internal organ involvement

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

what are common drugs that can cause DRESS

A

allopurinol and anticonvulant

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

what is SJS/TEN

A

progressive bullous/ blistering disorders that constitute as dermatological emergencies, progress to include mucus membrane erosion and epidermal detachment

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

how to differentiate between SJS and TEN

A

<10% SJS, >30% TEN

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

what are common drugs that can cause SJS/TEN

A

abx especially sulfonamides

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

what is the treatment for SCAR

A

mostly supportive care (wound care, temperature regulation, nutritional support, pain management, fluids, prevention of infection)

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

what are the drugs that are susceptible to genetic predisposition for drug hypersensitivity

A

allopurinol. abacavir, carbamazepine, phenytoin

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

what are autoimmune diseases

A

when body is attacked by own immune system

44
Q

what are examples of autoimmune diseases

A

rheumatoid arthritis, type 1 DM, grave’s disease, systemic lupus erythematous, systemic vasculitis, scleroderma, psoriasis, sjogren’s syndrome, multiple sclerosis

45
Q

what is systemic lupus erythematosus

A

autoimmune disease associated with autoantibody production, is a multisystem disease

46
Q

what are the characteristics of SLE

A

more prevalent in females, strong genetic predisposition and environmental factors

47
Q

what is the pathophysiology of SLE

A

characterised by disorders of the innate and adaptive immune system, T and B cell signalling altered in SLE which causes abnormal clearance of apoptosis debris containing nuclear material which can stimulate immune responses, number of plasma cells increased in active SLE which increases number of Ab produced which causes tissue damage

48
Q

what are the git clinical presentation of SLE

A

mouth and nose ulcers

49
Q

what are the skin clinical presentation of SLE

A

butterfly rash, red patches

50
Q

what are the respiratory clinical presentation of SLE

A

pleuritis, pneumonitis, pulmonary emboli, pulmonary hemorrhage

51
Q

what are the cardio clinical presentation of SLE

A

endocarditis, atherosclerosis, inflamm of fibrous sac

52
Q

what are the blood clinical presentation of SLE

A

high BP, anemia

53
Q

what are the kidney clinical presentation of SLE

A

blood in urine

54
Q

what are the muscle and joints clinical presentation of SLE

A

pain, arthritis aches, swollen joints

55
Q

what are the other clinical presentation of SLE

A

hair loss, abnormal headache, high fever

56
Q

what is lupus nephritis

A

lupus Ab affect structures in kidneys which help filter out waste, kidneys affected to different extents (class I to VI)

57
Q

what is neuropsychiatric lupus

A

lupus affect brain, spinal cord and other nerves

58
Q

what are the full blood count biomarkers and should it be low or high in SLE

A

decr RBC due to hemolytic anemia, decr WBC and lymphocytes, decr PLT

59
Q

what are the immunological biomarkers and should it be low or high in SLE

A

positive antinuclear Ab (ANA), positive anti ds-DNA (dsDNA), positive antinuclear ribonuclearprotein (antiRNP), antismith Ab (anti-Sm), low complement (C3, C4, CH50)

60
Q

what does positive ANA mean

A

immune system launch a misdirected attack on own tissue

61
Q

what does positive anti-RNP suggests

A

connective tissue disease

62
Q

why would there be low complement in SLE

A

due to activation of complement system in SLE (type III hypersensitivity)

63
Q

what is the general treatment goals for SLE

A

goal to achieve remission but realistically to aim for low disease activity, to prevent flares, reduce use of steroids, improve QoL, minimise adverse effects, evaluate and treat comorbs, lifestyle and support groups

64
Q

what are the approved FDA drugs for pharmacological treatment of SLE

A

aspirin, prednisolone, hydroxychloroquine, belimumab

65
Q

what are the drug classes and its uses (and caution if any) for pharmacological treatment of SLE

A

NSAIDs - first line agent for acute symptoms, caution in lupus nephritis, increased cardiac risk and GI bleed

steroids - mono/ adjunct therapy to prevent flares and maintain low disease activity, has rapid onset, caution with long term use

biologics - target and disrupts functioning of B cells

immunosuppressants

66
Q

what is the chosen drug for treatment of SLE (moa and duration of use)

A

all patients with SLE to take hydroxychloroquine due to its anti inflamm, anti thrombotic and immunomodulatory effects, has minimal adverse effects and to be used for 4-8w

67
Q

what are examples of immunosuppressants used for treatment of SLE

A

IV/PO cyclophosphamide, mycophenolate, azathioprine

68
Q

what is cyclophosphamide used for in SLE

A

severe organ involvement as induction therapy

69
Q

what is mycophenolate used for in SLE

A

induction and maintenance therapy

70
Q

what is azathioprine used for in SLE

A

alternative to mycophenolate for maintenance

71
Q

how do you evaluate the therapeutic outcome for SLE

A

ADR, comorbs, biomarkers, disease progression based on questionaires

72
Q

what are the questionaires used to measure disease activity

A

SELENA-SLEDAI, BILAG

73
Q

how often are lab tests conducted for SLE

A

q1-3m if active, q6m if stable

74
Q

what are the biomarkers in the lab tests for SLE

A

anti-dsDNA, CRP, FBC, complement, urinalysis/ renal func, LFTs

75
Q

what are the biomarkers that do not need to be repeated every session for SLE

A

anti-RNP, ANA, antiSm

76
Q

what is antiphospholipid syndrome

A

antiphospholipid antibodies are present, which act as inhibitors and bind to phospholipid in clotting factors thus increasing the risk of clotting and thrombosis

77
Q

what are the three primary antiphospholipid Ab

A

lupus anticoagulant, anticardiolipin, anti-beta glycoprotein 1

78
Q

what is the treatment for APS

A

primary thromboprophylaxis using hydrochloroquine, aspirin
secondary thromboprophylaxis using warfarin

79
Q

what are the drugs of high risk that can cause drug induced lupus

A

procainamide, hydralazine, quinidine

80
Q

what are the other drugs that can cause drug induced lopus

A

methyldopa, carbamazepine, isoniazid, minocycline

81
Q

what is the potential moa of drugs that causes drug induced lopus

A

small molecules that induce an immune response by binding to larger molecules like proteins

82
Q

what is the treatment for drug induced lupus

A

stop use and consider symptomatic treatment

83
Q

what is the goal for induction treatment to achieve immunosuppression

A

high potency and short course treatment asap to reduce existing damage and prevent worsening of autoimmune condition

84
Q

what are the drugs used in induction therapy and how does it achieve immunosuppression

A

prevent acute rejection with lymphocyte depleting therapy using basiliximab and alemtuzumab

85
Q

what are the drug classes used in maintenance therapy to achieve immunosuppression

A

corticosteroids, calcineurin inhibitors, mTOR inhibitors, antimetabolites, biologics

86
Q

what are examples of drugs that are calcineurin inhibitors

A

cyclosporin, tacrolimus

87
Q

what are examples of drugs that are mTOR inhibitors

A

sirolimus, everolimus

88
Q

what are examples of drugs that are antimetabolites

A

mycophenolate, azathioprine

89
Q

what are examples of drugs that are biologics

A

adalimumab

90
Q

what are the complications of immunosuppression

A

opportunistic infections, cancer, renal toxicity, hepatotoxicity, blood disorders, cardio complications (htn, hyperlipidemia, hyperglycemia)

91
Q

what are the types of opportunistic infections that can result from immunosuppression

A

bacterial, viral, fungal, parasites

92
Q

what are the drugs that can cause renal toxicity

A

calcineurin inhibitors (tacrcolimus, cyclosporin)

93
Q

what are the drugs that can cause hepatotoxicity

A

antimetabolites (mycophenolate, azathioprine)

94
Q

what are the blood disorders as a result of immunosuppression

A

thrombocytopenia, leukopenia, pancytopenia

95
Q

what are the drugs that can cause hyperglycemia

A

mTOR inhibitors (sirolimus, everolimus), calcineurin inhibitors (tacrolimus, cyclosporin)

96
Q

what is thrombocytopenia

A

low PLT

97
Q

what is leukopenia

A

low WBC

98
Q

what is pancytopenia

A

low WBC, RBC, PLT

99
Q

what are the therapeutic effects of steroids

A

DMARD effect in RA, anti inflamm and immunosuppression (decr pain, swelling, physical disability, stiffness), anti allergic, decr endothelial permeability and dysfunction

100
Q

what are the adverse effects of steroids

A

incr cvs risk, cataract glaucoma, hirsutism and skin thinning, gastric ulcer if concomitant NSAIDs, weight gain, fluid retention, cushing syndrome, impaired glucose metabolism, insulin resistance, beta cell dysfunction, neuropsychiatric symptoms, HPA insufficiency, osteonecrosis, osteoperosis, myopathy, infections

101
Q

what does HPA stand for

A

hypothalamus-pituitary-adrenal

102
Q

who is most susceptible to HPA axis suppression

A

patients on chronic corticosteroid therapy

103
Q

what is the process of HPA axis suppression

A

exogenous glucocorticosteroids causes decr secretion of CRH and ACTH due to negative feedback -> over time leads to atrophy of HPA axis due to inactivity -> results in adrenal suppression

104
Q

what is CRH and where is it secreted from

A

corticotropin-releasing hormone from hypothalamus

105
Q

what is ACTH and where is it secreted from

A

adrenocorticotropic hormone from pituitary

106
Q

what is the approximate cut off of steroid use to prevent adrenal suppression

A

> 5mg prednisolone equivalents daily for more than 3w

pr3152 (6 decks)

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