Week 4 Flashcards
1
Q
Type 1 hypersensitivity
- name
- mediated by
- cells involved
A
- immediate hypersensitivity
- mediated by IgE
- Mast cells
2
Q
Type 2 hypersensitivity
- mediated by
- cells involved
- occurs in solution?
A
- IgG but can sometimes be IgM
- none; the antibodies are directed against tissue
- no
3
Q
Type 3 hypersensitivity
- mediated by
- describe what mediates it
- occurs in solution?
A
- immune complexes
- Antigen, antibody, and complement
- yes
4
Q
Type 4 hypersensitivity
-mediated by
A
-T cells
5
Q
Hygiene hypothesis
- what is it?
- why does it occur?
A
- epidemic of type 1 hypersensitivity in developed countries
- body doesn’t get experience that it needs and is not exposed to diff pathogens because we have vaccines, antibiotics, and clean water to bathe in
6
Q
IGE and parasites
A
- IgE is supposed to protect body against parasites
- parasites are more similar to humans and have less antigenic properties
- parasites are not killed by macrophages/neutrophils (too big)
- attached to mast cells, basophils, eosinophils which will produce concerted mast-cell degranulation and violence dislodges embedded parasites from the tissues and ejects them
7
Q
IgE and IgG3 in early immune response
A
- primary response to an antigen, IgM is first switched either to IgG or IgE
- IgG will then differentiate into 1 of 4 subtypes, with IgG3 being located first in gene
- both IgE and IgG3 are short lived and favor complement fixation, mast cell degranulation, and phagocytosis
8
Q
What isotype of antibodies would be prevalent in atopic individuals
A
- IgG3
- Starts out as IgM and then goes to IgE or IgG
9
Q
IgG1, 2, and 4
A
- longer-lived,
- increasingly less inflammatory,
- favor the formation of immune complexes
10
Q
Isotype switching going back to IgE
A
Some B cells making high-affinity IgG, particularly IgG4, can switch to IgE at a late stage in the germinal center reaction.
11
Q
IgE details
A
- not retained in blood, concentrated in tissue
- binds to FcεRI
- bent, asymmetrical ‘shrimp-like’ structure
- Fab arms have less movement
- highest affinity for antigen and irreversible binding
- can bind to its receptor without antigen bound first; this causes for it to better express binding site for antigen
12
Q
IgE, FcεRI, mast cells and memory
A
- all IgE that did not get bound during infection will get bound to mast cell by FcεRI receptor and serve as memory cells
- there are a bunch of IgE molecules on mast cells with different specificity
13
Q
FcεRII (CD23)
A
- role in the production of IgE and its maintenance in the circulation
- conformation of the IgE Fc region that permits binding to FcεRII has no affinity for FcεRI
- binds with low affinity
- when two or three binding sites on FcεRII are occupied by immune complexes of IgE and antigen, the binding strength approaches that of FcεRI.
14
Q
ADAM10
A
- cleave CD23
- to produce either monomeric or trimeric forms of soluble CD23
15
Q
Soluble form of CD23
A
- have cytokine-like activities that act in an autocrine or paracrine fashion
- effects are wide-ranging
- expressed in b-cells, T cells, monocytes, follicular dendritic cells, and bone marrow stromal cells
16
Q
B cell, IgE, and CD23
-monomeric vs trimeric
A
- when B cell expresses IgE it begins to shed CD23
- absence of antigen, complex of soluble trimeric FcεRII interacts with B-cell receptor (surface IgE) and B-cell co-receptor which generates synergistic signaling that promotes the differentiation of the B cell into an IgE-secreting plasma cell
- monomeric form of soluble FcεRII inhibits such differentiation.
17
Q
Mast cells and tissue they live in
A
- resident in mucosal, epithelial tissue, and all vascularized tissues except the central nervous system and the retina
- maintain the integrity of the tissue where they reside by alerting the immune system to local trauma and infection, and facilitating the repair of damage caused by infection or wounds.
18
Q
Mast cells
A
- best known for destructive properties of their granules
- express Toll-like receptors; Fc receptors for IgA, IgG, and IgE.
- contribute to both the innate and the adaptive immune responses to infection
- create eicosanoids
- two kinds
19
Q
eicosanoids
A
- small inflammatory mediators
- induces the productions and secretion of cytokines that recruit neutrophils, eosinophils, and effector T cells to the infected tissue, and also induces the secretion of growth factors that promote the repair of tissue damage.
20
Q
mucosal mast cell
A
- produces the protease tryptase
- depends on the effector T cells
21
Q
connective tissue mast cell
A
produces chymotryptase.
22
Q
eosinophils
- what kind of cell
- where are they resident
- what happens when body is healthy
- what activates it?
- function?
- what induces degranulation?
- what allows for them to bind pathogen?
A
- granulocytes whose granules contain arginine-rich basic proteins
- tissues specifically in CT under epithelia of respiratory, GI, and urogenital tract
- activation leads to the staged release of toxic molecules and inflammatory mediators
- kill invading microorganisms and parasites directly and induce synthesis and secretion of prostaglandins, leukotrienes, and cytokines, which amplify the inflammatory response by the activation of epithelial cells and leukocytes, including more eosinophils
- number of eosinophils is kept low by restricting their production in the bone marrow
- IL-5 from TH2 cells
- expression of FcεRI and binding IgE
- Fcγ receptors (to bind to IgG) and complement receptors
23
Q
Basophils
- cell type
- growth factors
- relationship with eosinophils
- role in adaptive immunity
- function
- effect on B cells
A
- granulocytes
- growth factors, including IL-3, IL-5, and GM-CSF
- TGF-β and IL-3 pro- motes the maturation of basophils while suppressing that of eosinophils
- key cell that initiates TH2 responses by secreting IL-4 and IL-13
- function is to degranulate in infected tissue and recruited to secondary lymphoid tissue to secrete IL4 and 13
- drives isotype switching to IgE and IgG4 by binding to CD40 on antigen-stimulated B cell
24
Q
Mast cells, basophils, and Eosinophil effect on eachother
A
- Mast-cell degranulation initiates the inflammatory response, which recruits eosinophils and basophils.
- Eosinophil degranulation releases major basic protein which causes degranulation of mast cells and basophils which is augmented by one or more of the cytokines—IL-3, IL-5, and GM-CSF—that affect the growth, differentiation, and activation of eosinophils and basophils
25
Effector mechanism for type I hypersensitivity
- triggered by the interaction of an allergen with allergen-specific IgE bound to the FcεRI receptor of mast cells, basophils, and eosinophils.
- interaction causes these cells to degranulate and release a potent mixture of inflammatory mediators
26
Effector mechanism for type II hypersensitivity
- caused by an IgG response to chemically reactive small molecules that become covalently bound to the outside surface of cells
- chemical reaction modifies the structures of human cell-surface components, which are now perceived as foreign antigens
- B cells are stimulated to make IgG antibodies which cause cause the modified human cells to become subject to complement activation and phagocytosis
27
Effector mechanism for type III hypersensitivity
- caused by small soluble immune complexes of antigen and specific IgG that form deposits in the walls of small blood vessels or the alveoli of the lungs
- immune complexes activate complement and an inflammatory response that damages the tissue and impairs its function.
28
Effector mechanism for type IV hypersensitivity
- mediated by antigen-specific effector T cells, and in most instances by CD4 TH1 cells
- Peptides containing the residues are presented by HLA class II molecules and recognized as non-self by CD4 T cells that respond by attacking any area of the skin that comes into contact with antigen
- Some type IV hypersensitivity reactions are due to CD8 T cells (poison ivy)
29
How are allergens picked up?
dried up particles that are inhaled
30
What is the first exposure to an allergen called?
- sensitization
- first exposure to an allergen, you're gonna make the antibodies, the antibodies have not been able to arm the mast cells yet and mast cells cannot degranulate and cause terrible allergic response.
31
sensitization and mast cells
- extraction of the antigen, it gets into the mucus, it will be solubilized, then gets into the APCs, it presents it to a Helper T cell (Th2), which will induce the B cell to make IgE.
- In the first response the IgE will be directed against the antigen, but everything that is left over that initial response gets taken up by mast cells, basophils, and eosinophils
- During sensitization, you have the weakest response in the first exposure bc mast cells will not have been armed with IgE
32
immediate and late-phase response
- immediate: wheal and flare; direct consequence of IgE- mediated degranulation of mast cells in the skin; Released histamine and other mediators cause increased permeability of local blood vessels, where- upon fluid leaves the blood and produces local swelling (edema). The swelling produces the wheal at the injection site, and the increased blood flow into the surrounding area produces the redness that is the flare. Immediate reactions can last for up to 30 minutes, and the relative intensity of the wheal and flare varies.
- 6–8 hours after the immediate reaction; more widespread swelling and is due to the leukotrienes, chemokines, and cytokines synthesized by mast cells after IgE-mediated activation
33
Allergic reaction and lungs
On inhalation of an allergen to which a patient is sensitized, mucosal mast cells in the respiratory tract that are armed with allergen-specific IgE will degranulate. The released mediators cause immediate constriction of the bronchial smooth muscle, which results in the expulsion of material from the lungs by coughing, and difficulty in breathing. It induces the recruitment of leukocytes, particularly eosinophils and TH2 lymphocytes, into the site and, if antigen persists, the late-phase response can easily develop into a chronic inflammatory response in which allergen-specific TH2 cells promote IgE production and a state of eosinophilia
34
What is the effect of leukotrienes
- cause pain, inflammation, dilation, bronchoconstriction
| - are a lot more potent than histamine
35
IgE allergic reactions vary by tissue type
- gut: interactions between antigen, IgE, and mast cells trigger violent muscular contractions that can expel worms from the gastrointestinal tract and increase fluid flow to wash them out
- lungs: muscular spasms and increased secretion of mucus that result from mast-cell activation can be seen as a way to expel organisms
- blood vessels: increase blood flow and permeability causes increased flow of antigens in lymph to lymph nodes
36
Penicillen and anaphylactic shock
- β-lactam ring can be opened up to produce covalent conjugates with proteins of the body, creating new ‘foreign’ epitopes
- response is dominated by TH2 cells that help B cells produce IgE specific for the new epitopes.
- If penicillin is given to a person who has been sensitized in this manner, it causes anaphylaxis and even death
37
Systemic anaphylaxis
- allergen enters the bloodstream and cause widespread activation of the connective tissue mast cells associated with blood vessels
- causes an increase in vascular permeability and a widespread constriction of smooth muscle.
- causes the blood pressure to drop drastically and CT to swell
38
Epi and anaphylaxis
Epinephrine stimulates the reformation of tight junctions between endothelial cells. This reduces their permeability and prevents fluid loss from the blood, diminishing tissue swelling and raising blood pressure. Epinephrine also relaxes constricted bronchial smooth muscle and stimulates the heart
39
allergic rhinitis
-also called hay fever
- caused by allergens that diffuse across the mucous membrane of the nasal passages and activate mucosal mast cells beneath the nasal epithelium
- characterized by local edema, leading to obstruction of the nasal airways and a nasal discharge of mucus that is rich in eosinophils. There is also a generalized irritation of the nose due to histamine release.
-
40
allergic asthma
- allergic reactions cause chronic difficulties in breathing, such as shortness of breath and wheezing.
- triggered by allergens activating submucosal mast cells in the lower airways of the respiratory tract. Within seconds of mast-cell degranulation there is an increase in the fluid and mucus being secreted into the respiratory tract, and bronchial constriction caused by contraction of the smooth muscle surrounding the airway.
- overall effect of the asthmatic attack is to trap air in the lungs, making breathing more difficult
41
chronic asthma
- chronic inflammation that develops after allergic asthma perpetuated in the absence of further exposure to the allergen.
- airways can become almost totally occluded by plugs of mucus
- airways hyper-reactive to chemical irritants commonly present in air
- condition is exacerbated by immune responses to bacterial or viral infections of the respiratory tract
- classified as type IV hypersensitivity response
42
allergic reactions in the skin
- Allergens that activate mast cells in the skin to release histamine cause raised itchy swellings called urticaria or hives
- Activation of mast cells in deeper subcutaneous tissue leads to a similar but more diffuse swelling called angioedema
- prolonged allergic response in the skin is called atopic dermatitis or eczema; believed to be due to loss of the protective barrier function of the skin, allowing allergens to enter the skin and stimulate a TH2-cell mediated immune response
43
effects of ingested allergens
- IgE is made against an extremely small proportion of proteins ingested.
- Foods that commonly cause allergies include grains, nuts, fruits, legumes, fish, shellfish, eggs, and milk
- allergen passes across the epithelial wall of the gut and binds to IgE on the mucosal mast cell which causes degranulation. Local blood vessels become permeable, and fluid leaves the blood and passes across the gut epithelium into the lumen of the gut. Meanwhile, contraction of smooth muscle of the stomach wall produces cramps causing vomiting and diarrhea
44
Most commonly transplanted tissue
blood; which can cause hypersensitivity reaction
45
Hypersensitivity and blood transfusion
- need to check for blood group antigens and rheus D antigen
- if blood with wrong antigens are transfused IgG will bind to it and cause complement fixation and rapid clearance of the red cells from the circulation
- we make antibodies from A, B antigens on common commensal bacteria that have structural similarity to our own cell-surface carbohydrates
46
Rejection of transplanted organs
- ABO antigens are present on the endothelial cells of blood vessels as well as on erythrocytes. So if organ is from patient with different type blood then antibodies in recipients circulation will bind to the vessels of the graft (hyperacute rejection, type II hypersensitivity). inflamed state of the transplanted organ activates the organ’s dendritic cells. These donor-derived dendritic cells migrate to the draining secondary lymphoid tissue, where they settle into the T-cell zone and present complexes of donor MHC and donor self peptides to the recipient’s circulating T cells.
- preexisting antibodies against HLA class I variants can also cause hyperacute rejection.
- cross-match test, in which blood serum from the prospective recipient is assessed for the presence of antibodies
47
What can cause anti-HLA antibodies
- pregnancy: fetus expresses paternal HLA allotypes that are not part of the mother’s HLA type and have the potential to stimulate an alloreactive immune response. During child birth cells and material of fetal origin enter the maternal circulation and stimulate an immune response. Antibodies can be made against any paternal HLA allotype expressed by the baby and not by mother. successive pregnancies, increasing levels of anti-HLA antibodies can develop.
- blood transfusion: In routine blood transfusion, HLA type is not assessed, the matching being restricted to just the ABO and Rhesus D types. Infusion of HLA-incompatible leukocytes and platelets in a blood transfusion can therefore generate antibodies specific for the donor HLA allotypes.
48
Alloreactions
- immune response against MHC1 (alloantigens)
- transplant rejection: recipient attacks donor organ
- graft vs host reaction: The major alloreactions that occur after hematopoietic cell transplantation are due to donor T cells in the graft that respond to and attack the recipient’s healthy tissues.
49
Chronic rejections
- Type III hypersensitivity that involve immune complexes
- will happen over months or years
- antigen in immune complexes are MHC1
- caused by donor DC migrating to lymph node and activating recipient T-cells to attack donor organ
50
Direct vs indirect allorejection
direct: caused by donor DC migrating to lymph node and activating recipient T-cells to attack donor organ
- indirect: some of the donor-derived dendritic cells migrate to draining lymphoid tissue and die there by apoptosis. Membrane fragments containing HLA molecules from apoptotic cells are taken up by dendritic cells of the transplant recipient and processed so that peptides derived from donor MHC are presented by the recipient’s MHC II activating T cells
51
Serum sickness
-type III hypersensitivity
- injection of large amount of
an antigenic protein, (mouse
monoclonal antibody) into
circulation leads production of antibody which form immune complexes with the antigen, and complexes are deposited in small blood vessels and activate
complement and phagocytes, inducing
fever and the symptoms of vasculitis, nephritis, and arthritis
-effects are transient and resolve
once the antigen has been cleared
52
Dermatographia
put some physical stimulation to the skin, you can write on their skin in patients with atopia
53
Angioedema
- local or systemic?
- mediated by?
- occurs with?
- difference with urticaria
- etiology
- airway
- Sudden localized nonpitting edema of skin and submucosa of mouth, throat, or GI tract
- Mediate by IgE
- Whole body reactions as a result to exposure to various antigens
-Frequently occurs with urticaria
-difference between angioedema and urticaria?
Urticaria itches, Angioedema doesn’t
-etiology: idiopathic, congenital, IgE mediated, rxn to ACE inhibitor
-dysphagia, voice changes, difficulty breathing
54
Allergy emergencies
- Asthma: acute attack
| - Anaphylaxis: whole body reaction
55
anaphylactic reaction vs anaphylactoid reaction
- anaphylactic you're dealing with IgE mediation in anaphylactoid IgE is not involved
- They look exactly the same, both lead to anaphylaxis
56
Anaphylaxis and genders
-males have higher risk up to 15 yrs old, then females will have higher risk
57
Effects of anaphylaxis
- increased bronchial muscle tone
- increased mucus membrane secretion
- decreased vascular tone
- capillary leakage
- urticaria
58
Treatment of anaphylaxis
-IM epi; 33-66 lbs=.15 mg; 66 lbs and up= 0.3 mg
59
Anaphylactoid reactions
-direct stimulation of mast cells (opiates, contrast), disturbances of arachadonic acid metabolism (NSAID, aspirin), physical stimuli (cold/exercise)
60
Types of transfusion reactions
- Acute hemolytic reaction: Red cells are being lysed, Type 2 reaction
- Febrile non-hemolytic reaction: Most common form; Blood has been taken from someone, put in cold storage, blood deteriorates after some time and so mediators are released into the blood, and when transfusing you have the mediators floating around in you; not an ABO incompatibility, its is a result of the mediators being released, Fresh whole blood will have a low incidence of this
- Delayed hemolytic reaction
- Transfusion-related lung injury
61
Order of safety for transfusions
- autologous blood
- typed/crossed/washed RBCs
- typed/crossed RBC's
- typed RBC's
- O negative
62
Role of arterioles
- Site of oxygenated blood
| - Regulates flow with constriction and dilation into the capillary system
63
Structure of arterioles
- Smooth muscles
| - Endothelial cells
64
Arterial tone
○ How tight the smooth muscle is at baseline
○ Shape of vessel
○ Compliance: stretchy
○ Elasticity: ability to come back to shape
○ Tone ability to maintain shape
65
Sepsis and compensatory response
BP: low
HR: high (compensatory for BP)
RR: high
66
Why give IV with sepsis
- Expand volume to increase BP so that more oxygen is supplied to tissue
○ Hypovolemic anemia
67
What causes low BP
- TNF alpha is binding to blood vessels to open them up
- Will increase NO by increasing NOS
- alters tight junctions in endothelial cells, allowing for increased permeability
- Plasma protein is increasing because of holes in vasculature
68
How to dilate vessels
NO or cAMP
69
Why are extremities cold in sepsis
Shunting blood to vital organs
70
Function of histamine
Vasodilates the arterioles by increasing cAMP
71
Why would someones have trouble breathing with anaphylaxis
Constriction of smooth muscles in respiratory tract
72
How do we know that anaphylaxis is systemic problem
BP is low ,systemic vasodilation
73
How does epi work
Causes vasoconstriction and relaxation of smooth muscle in respiratory tract
74
Why give antihistamine for anaphylaxis
It is antagonist of histamine receptor which prevents histamine from doing its job
75
Why give corticosteroid for anaphylaxis?
To suppress immune response
76
What is significant about timing of delayed hypersensitivity rash?
usually starts 7- 10days after drug is initiated
77
Risk for drug reaction
- Females have 1.3-1.5 % greater risk of drug reaction
| - Children less than 3 boys have greater risk
78
How common are exanthematous drug eruptions
- most common presentation of skin rashes related to drugs (90%)
- IgG mediated
- Limited to skin, not involving organs
- TMP-SMX is common drug for this type of reaction
79
Management of exanthematous drug eruptions
- Step 1: discontinue medication
- Step 2: treat sxs
- Step 3: substitute medications (continue to treat infection causing UTI)
80
TMP-SMX drug reactions
sulfa moiety causes the rxn
81
additional drugs with sulfa-moiety
- Anti-convulsants/epileptics: Carbamazepim
- Cox 2 inhibitors
- Diuretics
- Antibiotics with sulfa
82
What other drugs can be used instead of TMP-SMX
- Cephalosporins (1st or 3rd generation): Amoxicillin
- Beta-lactams: Penicillin, cephalosporin
- Nitro-furitonin: Specific for UTI
- Any antibiotic that does not have sulfa group in it
83
When would you continue medication that causes drug reaction
- Medication causing reaction is only treatment for bacterial infection, especially if infection is life threatening if the symptoms aren't too severe
84
How do you treat rash with drug reactions
- Topical corticosteroids: because local infection
- Oral anti-histamine
- Cold/warm compresses
- Oatmeal baths
- Reassure and educate patient that the rash will go away and sxs will pass--also what to avoid so this doesn't happen again
85
Difference between rash being caused by virus and and drug reaction
rashes caused by viruses are NOT itchy
86
Side effects of topical steroids
- Thinning of skin
| - Rosacea
87
What is induction of drug tolerance and when would you use
- only used with medications that are needed for life threatening diseases (ex- aspirin for cardiovascular disease)
- Giving small doses of drug to build tolerance to drug--only used with minimal reaction
88
antihistamines
- H1 antagonists only (Actually inverse agonists-- competing with indogenous histamine and outcompeting it)
- Outcompetes histidine in binding to H1
89
Where are H1 and H2 receptors located
○ Highest density of H1: Bronchiole, blood vessels, intestinal smooth muscle
○ High density of H2: predominately in GI but also in cardiovascular and immune cells
90
Difference between 1st and 2nd generation anti-histamines
H1 antagonists that are 2nd generation does not cross blood brain barrier because they have decreased lipophilicity and there are p-glyco-proteins that keep pushing them out of CNS
91
What do you do prior to EMS arriving during Type I hypersensitivity causing anaphylaxis
Antihistamine and epi-pen if you had access
92
commonly reported meds that causes anaphylaxis
- Penicillin
- Aspirin
- NSAIDS
- Insulin
93
Why give Epi IM to thigh
Because it is highly vascularized and can get into system faster
94
Antihistamines and anaphylaxis
- Both H1 and H2
- Diphenhydramine: H1 inhibitor
- Ranitidine: H2 inhibitor
95
Why isn't anti-histamine 1st line treatment for anaphylaxis
- Cannot help with broncho constrictors : involves leukotrienes (prostaglandins) which are extremely potent and mediating effect which can only be inhibited with Epi
- Give antihistamines at end to help with itching and swelling after breathing is controlled
96
Timeline of anaphylaxis
- First thing that happens is histidine is released but then prostaglandins (leukortiens) are released
- Usually prostaglandins would be released in second phase of allergic reaction (8 hours after exposure); however, in anaphylaxis the timeline gets pushed up for the reaction because of how sensitive they are to antigen
97
DRESS
- Drug rash with eosinophilia and systemic symptom
- Depending on drug will have variation of how many eosinophils and what organs are involved (liver, kidneys, eosinophils)
- Do NOT need to do skin biopsy for this
98
Risk factors of DRESS
- Female
- Previous hx of drug reactions
- Current drug exposure
- HLA type : Certain individuals will have heightened reaction to certain medication; very specific to individual and drug
- Gene type a patient who is going to start an anti-convulsant/epilectic (Especially carbanazopine)
- Common in patients with asian, northern asian, and euorpen descent with allele expression
99
Non-pharmaceutical Management for DRESS
- Discontinue offending agent and non-essential drugs
- Refer for derm consult
- Educate patient- tell patient about drug and side effects
100
Agents reported to cause DRESS
- Allopurinol; Sulfa and peinicillen
- Antibiotics: Sulfa, penicillen
- Anti-TB: isoniazid
- Anticonvulsants: Phenytoin, carbamazeoine, and lamotrigine
- NSAIDs: Meloxicam and diclofenac
- Anti-HIV agent: abacivir
101
Pharmaceutical treatment of DRESS
- Without organ involvement use topical cortiosteroid 2-3x a day for a week
- With organ involvement use systemic steroid
- Make sure to substitute the anti-convulsant
- Use palliative care for sxs
102
Important Sxs of DRESS
-facial edema
103
Important sxs of Stephen's-Johnson's syndrome
- Painful
- Will present with flu-like symptoms in addition of fever and rash
- Symptoms occur weeks after starting meds
- Erosions to mucous membrane
104
How does rash from Stephen's-Johnson's syndrome spread?
- normally starts in face and trunk and rapidly spreads to rest of body
- Peak of rash is 4 days
- Will do skin biopsy
- If over 25% of body will submit to burn unit
- Takes 3 weeks to re-grow skin if you survive
105
Treatment of Stephen's-Johnson's syndrome
- Discontinue offending agent
- Potentially going through burn unit
- Supportive care
- Anti-septic solution
- Sterile handling
- Nutrition and pain management
106
Why is sterile handling important in Stephen's-Johnson's syndrome
○ secondary bacterial infection
- Would not give topical gluco-corticoids with bacterial infection because it is immunosuppressant and will cause bacterial infection to get worse
107
Why is nutrition and pain management important in Stephen's-Johnson's syndrome
○ Very painful because of skin sloughing off: Use NSAIDS with codeine added or low efficacy opioid depending on how severe pain is
108
certain groups of people that have higher risk of Stephen's-Johnson's syndrome
○ There are genetic HLA genes that determine this
- Should do genetic testing before prescribing some of these medications (SATAN) especially if patient is going to be on them long term
109
Symptoms of seasonal allergies
- rhinorrhea
- itchy/sore throat
- sneezing
- watery eyes
- frontal headaches
- fatigue
- no fever
- post nasal drainage
110
decongestant MOA
- stimulate the alpha-adrenergic receptors to constrict dilated arteries within the nasal mucosa. This decreases the amount of swelling and formation of mucus in the nose
- example: mucinex
111
leukotriene receptor antagonists MOA
binding to cysteinyl leukotriene (CysLT) receptors and blocking their activation and the subsequent inflammatory cascade
