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hypersensitivity reactions Flashcards

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1
Q

how many types of hypersensitivity reactions are there?

A

4

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2
Q

what is a hypersensitivity reaction?

A

an excessive immune response

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3
Q

type 1 hypersensitivity reaction

A

allergic

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4
Q

what mediates type 1 hypersensitivity reactions

A

IgE

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5
Q

example of type 1 hypersensitivity reaction

A

allergic reaction to bee stings, latex, or certain medications like penicillin

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6
Q

type 2 hypersensitivity reaction

A

cytotoxic

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7
Q

what mediates type 2 hypersensitivity reactions

A

antibodies

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8
Q

example of type 2 hypersensitivity reactions

A

cytotoxic reactions like hemolytic reactions, goodpasture syndrome, or hyperacute graft reaction

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9
Q

what is type 3 hypersensitivity reaction?

A

immune complex deposition

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10
Q

what mediates type 3 hypersensitivity reactions?

A

IgG or IgM

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11
Q

example of type 3 hypersensitivity reaction

A

hypersensitivity pneumonitis, systemic lupus erythematosus, or serum sickness

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12
Q

type 4 hypersensitivity reaction

A

delayed

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13
Q

what mediates type 4 hypersensitivity reactions?

A

cells

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13
Q

example of type 4 hypersensitivity reactions

A

chronic graft rejections, PPD test, nickel, or poison ivy

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14
Q

mnemonic for remembering the order of hypersensitivity reactions

A

ACID

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15
Q

signs and symptoms of an anaphylaxis reaction

A

itching, tingling, coughing, difficulty breathing, weakness, dizziness, fainting, fear, nausea, vomiting, diarrhea, and facial/mucosal swelling

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16
Q

how do SaO2 levels change with an anaphylaxis reaction?

A

they decrease due to decreased BP

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17
Q

molecular pathway of anaphylaxis

A

first exposure causes IgE antibody to form, causing sensitized mast cells and basophils; upon second exposure, allergen binds to antibody, histamine is released, causing vasodilation, increased vessel permeability, and reaction to occur (redness, pruritus, and edema)

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18
Q

anaphylaxis definition

A

a severe, life-threatening, systemic hypersensitivity reaction (type 1) resulting in decreased BP, airway obstruction, and severe hypoxia

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19
Q

why does BP drop with anaphylaxis?

A

because of large increased in vasodilation

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20
Q

most common allergens for anaphylaxis

A

latex materials, nuts, insect stings, penicillin, anesthetics, and shellfish

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21
Q

what % of american population is anaphylaxis?

A

2%

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22
Q

who does anaphylaxis affect the most?

A

children and adolescents

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23
Q

risk factors for anaphylaxis

A

chronic asthma, acute exercise, fever, and stress; these all make mast cells more likely to degranulate due to release of cytokines

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24
2 serious problems of anaphylaxis
severe vasodilation causing a decrease in BP and edema in the lungs causing constriction of the bronchi and bronchioles; these combined pose a risk for a loss of consciousness
25
why does a loss of consciousness occur with anaphylaxis?
due to a lack of oxygen from the circulatory system (drop in BP) and respiratory changes (decrease in airflow)
26
3 criteria for anaphylaxis
1. acute onset involving skin and mucosal tissue 2. two or more of involvement of skin/mucosa, respiratory compromise, or GI symptoms 3. reduced BP (>30% reduction from normal)
27
how to treat anaphylaxis?
horizontal position (makes breathing easier and reduces risk of loss of consciousness) and inject epinephrine
28
role of epinephrine in anaphylaxis
vasoconstrictor that increases BP, RR, and HR
29
what anti inflammatories can be given to anaphylaxis that isn't improving?
chlorpheniramine and hydrocortisone; they decrease the mast cell response
30
antihistamines effect
inhibit formation of histamine or binding of histamine to receptors, has a slower action
31
example of an antihistamine
chlorphenamine
32
glucocorticoid role in anaphylaxis
broader anti inflammatory that has a slower effect
33
intravenous fluid role in anaphylaxis
increases BP and works fast
34
what to do as a PT with anaphylaxis?
seek emergency help ASAP, inject epinephrine, apply O2 if available
35
example of a type II reaction
myasthenia gravis
36
myasthenia gravis definition
is an acquired autoimmune deficit of acetylcholine receptors that impairs neuromuscular transmission, characterized by fatigable muscle weakness
37
two types of myasthenia gravis
generalized (about 80%) or ocular muscles (about 20%)
38
how antibodies are produced in MA?
antibody is produced and it binds to self cells, causing complement cascade to activate, which then binds to cell and damages cell, causing phagocytosis; essentially the system is reacting to own self cells
39
what does an antibody binding to a cell self result in?
complement cascade being initiated
40
who does myasthenia gravis affect the most?
children and adolescents
41
why is the prevalence of myasthenia gravis increasing?
because the population is growing and because treatment is improving, allowing those with this condition to live longer
42
risk factors for myasthenia gravis
can be precipitated by viral infections (infection activates immune system and antibodies that bind to ach) and is often associated with other autoimmune disorders
43
how does myasthenia gravis develop?
production of an antibody against the acetylcholine receptor that inhibits the receptor activity and leads to muscle cell death
44
signs and symptoms of myasthenia gravis
fatigable muscle weakness which are worsened with potential fatigable factors like heat or stress; other symptoms include diplopia (double vision), ptosis (eyelid drooping), and difficulty swallowing or breathing
45
how is myasthenia gravis classified?
5 classes
46
diagnosis of myasthenia gravis
blood test for antibodies against Ach, ice test (more sensitive), fatigability tests, repetitive nerve stimulation, and imaging (to rule out cancer of thymus)
47
how does the ice test work for myasthenia gravis?
acetylcholinesterase is inhibited at lower temperatures, so fatigability is improved due to slightly less improved Ach bindingw
48
why should you rule out thymus cancer when diagnosing myasthenia gravis?
because thymoma cells express an epitope that looks similar to Ach receptors, so immune cells may cross react
49
treatment for myasthenia gravis
treatable with anti-acetylcholinesterase medications and immunosuppressants
50
myasthenic crisis
is a risk in those patients with myasthenia gravis whose respiratory muscles are already weak, triggered by infection
51
what to do as a PT working with myasthenia gravis?
work alongside the medial team to monitor exercise levels, training respiratory muscles (inspiratory muscle training), helping develop strategies to manage condition, and assistance with management of respiratory complications
52
inspiratory muscle training
is breathing against resistance and is beginning to be used by PTs for myasthenia gravis
53
what is the view of exercising with myasthenia gravis?
is safe and improves neuromuscular parameters
54
example of a type III hypersensitivity reaction?
RA
55
pathophysiology of RA
antibody bind to antigens, forming immune complexes throughout the circulation which deposit in tissues or vessels, causing complement cascade to be activated, causing an inflammation and phagocytosis response and a chronic cycle of worsening inflammation
56
what is released in a RA response?
lysosomal enzymes and chemical mediators
57
stiffness in RA compared to OA
RA morning stiffness lasts longer than OA which gradually decreases in the morning; so key to ask patients about how long the stiffness lasts
58
two major types of arthritis
inflammatory (RA) and non-inflammatory (OA)
59
most common cause of inflammatory arthritis
rheumatoid arthritis
60
most common cause of non-inflammatory arthritis
osteoarthritis
61
pathophysiology of RA
immune system forms antibodies to self-antigens and DNA/RNA, forming antibodies that attack against self-antigens and immune complexes deposit, causing inflammation and tissue damage
62
what type of hypersensitivity reaction is RA classified as?
type III
63
criteria of RA
involves 3+ joints (often symmetrical), positive RF factors, positive CCP, elevated c-reactive protein, elevated ESR, excluded other diseases, and duration of 6+ weeks
64
peripheral polyarthritis meaning
RA affects not vertebral column but instead the peripheral joints and many of them (poly)
65
similar arthritis conditions similar to RA
psoriatic arthritis, acute viral polyarthritis, polyarticular gout, or systemic lupus erythematosus
66
zero negative RA
is negative rheumatoid factor but all other criteria are present for RA
67
what population does RA affect?
1% of the population, peak onset 30-55 years, and more common in females
68
risk factors for RA
diabetes mellitus, smoking, BMI (these are pro-inflammatory conditions), and genetic
69
what inflammatory cells are involved in RA reaction?
macrophages, lymphocytes, and synoviocytes, as well as many cytokines
70
what can RA lead to if not treated?
synovitis, pannus, cartilage erosion, fibrosis, ankylosis (joints fusing together), muscle atrophy, stretching of ligaments, altered joint alignment, and systemic effects
71
extra-articular manifestations of RA
accelerated atherosclerosis (MI, stroke, peripheral vascular disease) which leads to premature death, myocardial disease, coronary arteritis, pericarditis, and raynaud's syndrome
72
why is RA so important to treat?
because it can lead to premature death via accelerated atherosclerosis
73
who treats RA patients?
rheumatologist ASAP (usually 1-2 weeks); PTs can't prefer so refer to a MD who can then refer to rheumatologist
74
most important question to ask patients with RA?
prolonged morning stiffness?
75
signs and symptoms of RA
insidious onset, mild general aching and stiffness, inflammation often first noticed in fingers or wrists (symmetrical often), and worse in the morning but prolonged stiffness
76
why does stiffness with arthritis decrease after the morning?
movement helps to decrease pH levels which contribute to swelling and inflammation
77
diagnosis of RA
combination of clinical exam, history, and blood tests, as well as meeting the criteria, and imaging may be used to monitor progression
78
treatment for RA
refer to a rheumatologist and early use of disease modifying antirheumatic drugs (DMARDs), as well as use of NSAIDS and glucocorticoids
79
what medications are patients with mild RA given?
hydroxychloroquine and sulfasalazine and NSAIDs for rapid symptomatic relief
80
what medications are patients with moderate to severe RA given?
NSAID or glucocorticoids and DMARD therapy with methotrexate
81
what medications are RA patients given who are resistant to DMARD therapy?
a combination of DMARDs or switch to a different DMARD, while also treating the active inflammation (NSAIDs or glucocorticoid)
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