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AII week 1 > Clinical Medicine: Intro to Allergic Disease > Flashcards

Clinical Medicine: Intro to Allergic Disease Flashcards

1
Q

Etiology of anaphylaxis

A 
IgE mediated.  Caused by:
1. food
2. Pollen
3. Insect stings (venom)
4. Latex
5. Drugs
Nonimmunolgic: (mast cell degranulation, but not IgE mediated)
1. Exercise
2. Cold
3. Heat (sunlight/UV)
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2
Q

Clinical presentation of anaphylaxis (5-30min)

A
  1. CNS - lightheadedness, LOC, confusion, headache, anxiety
  2. Resp - SOB, Wheezes, pain with swallowing, cough, bronchodilation.
  3. GI - Cramping, diarrhea, vomitting
  4. Skin - hives, itchiness, flushing (90% of pts)
  5. Vascular - Hypotension, swelling, smooth muscle contraction
  6. Eyes - Swelling of conjuctiva
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3
Q

Category of RXN of anaphylaxis

A

Type I

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4
Q

Etiology of autoimmune hemolytic anemia

A

1/2 of cases idiopathic
- may also be associated with systemic lupus erythematous
Chronic lymphocytic leukemia
lymphomas. Caused by antibody induced hemolysis (destruction of RBCs) IgG or IgM mediated

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5
Q

Clinical presentation of hemolytic anemia

A
  1. May be asymptomatic
  2. Life threatening
  3. Looks like other anemias
  4. Fatigue, dyspnea
  5. Angina or HF
  6. Jaundice and splenomegaly may be present
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6
Q

Category of RXN of hemolytic anemia

A

Type II

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7
Q

Etiology of post streptococcal glomerulonephritis (PSGN)

A

Caused by prior infection with group A beta-hemolytic streptococcus (immune complex hypersensitivity). Complexes get trapped in glomeruli that causes an inflammatory reaction.

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8
Q

Who presents with PSGN most commonly

A

2-6yo with hx of pharyngitis(cold climate) and rash-impetigo (warm climate)

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9
Q

Clinical presentation of PSGN

A
  1. Most children asymptomatic
  2. Headache, malaise
  3. Anorexia, nausea, vomiting
  4. Flank/back pain - red urine
  5. Oligouria
  6. Elevated BP/edema
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10
Q

Category of RXN of PSGN

A

Type III

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11
Q

Etiology of serum sickness

A

Caused by antitoxins, antivenins, streptokinase, vaccines, insects. This then induces an antibody response and the formation of an immune complex. Causes tissue damage and vasculitis

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12
Q

Clinical presentation of serum sickness

A
  1. Pruritic rash - maculopapular or urticarial (hives)
  2. High fever
  3. polyarthritis
    Begins 7-10 days after exposure
    Usually goes away but could progress to angioedema, nephritis
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13
Q

Category of RXN of serum sickness

A

Type III

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14
Q

Etiology of vasculitis

A

Immune complexes are trapped in vessel walls. Leads to vessel injury. Primary - unknown cause. Secondary - infectious cause

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15
Q

Clinical presentation of vasculitis

A
  1. Fever, night sweats
  2. Fatigue, anorexia, weight loss
  3. Arthalgia/arthritis
  4. alveolar hemorrhage
  5. Mesenteric ischemia
    (some skin lesions
  6. Palpable purpura - small vessels
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16
Q

Category of RXN of vasculitis

A

Type III

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17
Q

Types of vasculitis (classification)

A
  1. Small vessel - Henoch-schonlein
  2. Medium vessel - kawasaki disease
  3. Large vessel - Giant cell temporal arteritis
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18
Q

Etiology of contact dermatitis

A
  1. Sensitization to an antigen
  2. Allergic response after reexposure
    Many causes - see chart in lecture notes pg 27
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19
Q

Clinical presentation of contact dermatitis

A 
Primary = intense pruritis
1. Transient erythema
2. vesiculations
3. Excoriation/infection
4. Swelling with bullae
Most common site is hands
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20
Q

Category of RXN of contact dermatitis

A

Type IV

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21
Q

Etiology of transplant rejection

A

Graft destruction caused by T cell-mediated reaction to allograft histocompatibility antigens

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22
Q

Clinical presentation of transplant rejection

A

Seen within days-few months post transplant

  1. Fever/chills
  2. Malaise
  3. Arthralgias
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23
Q

Category of RXN of transplant rejection

A

Type IV

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24
Q

What is the difference between anaphylaxis and anaphylactoid

A
  1. Anaphylaxis is mediated by IgE where as anaphylactoid is not
  2. Anaphylactoid can occur at 1st exposure, anaphylaxis cannot
  3. Skin test can only predict allergy in anaphylaxis
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25
Q

What is urticaria

A

Hives. A vascular reaction of the skin characterized by wheals surrounded by a red halo. PRURITUS!! is the main symptom.

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26
Q

What causes urticaria

A

Swelling of the upper dermis due to a mast cell reaction (IgE mediated) - can be secondary to anaphylaxis. Usually not longer than 12hrs.
(allergic rxn to food, worms, drugs -NSAIDS, penicillin, blood, IV contrast)

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27
Q

What is angioedema

A

Same manifestation as urticaria but it occurs in the deep dermis and subcutaneous tissue. Shows up as swelling more than wheals

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28
Q

Where is angioedema most commonly seen

A

Face and portion of an extremity. NOT pruritic. More painful or burning sensation. Seen in lips, cheeks, periorbital

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29
Q

What is hereditary angioedema (HAE)

A

Rare autosomal inherited blood disorder that causes swelling of face, extremities, genitals, GI tract and upper airway

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30
Q

What is acquired angioedema

A

Angioedema that occurs when there is a C1 inhibitor deficiency. C1 helps regulate the complement activation pathway. Result of allergy?

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31
Q

Etiology of allergic rhinitis

A

Caused by exposure to an airborne allergen in predisposed individuals (IgE response in addition to humoral and cytotoxic responses). IgE response, triggers mast cells (histamine) that migrate to the nasal epithelium.
Genetics, hygiene hypothesis, seasonal allergy

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32
Q

Clinical presentation of allergic rhinitis

A
  1. nasal congestion
  2. Rhinorrhea
  3. Sneezing
  4. Nasal Itching
  5. Pale or violet turbinates
  6. Conjunctival watering
  7. Postnasal drainage
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33
Q

Management of allergic rhinitis

A
  1. Intranasal corticosteroid sprays and systemic steroids
  2. Antihistamines - temporary/immediate relief
  3. Tailor the therapy to the individual
  4. Control environments - bed sheets, dust, clean
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34
Q

What is vasomotor rhinitis

A

Caused by an increased sensitivity of the vidian nerve and is the common cause of clear rhinorrhea in the elderly. Due to response of nasal stimuli (odors, scents, light)

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35
Q

Etiology of allergic conjunctivitis

A

Caused by seasonal allergens (usually hay fever related)

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36
Q

Clinical presentation of allergic conjunctivitis

A

Hyperemia and edema of the conjunctiva of the eye.

Will show up as red, itchy, swollen eyes

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37
Q

Management of allergic conjunctivitis

A
  1. Antihistamine
  2. Eye drops
  3. Air purifier
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38
Q

Clinical presentation of asthma

A
  1. Wheezing
  2. Dyspnea
  3. Chest tightness
  4. Cough
    (other symptoms may include urticaria, angioedema, erythema)
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39
Q

What causes asthma

A

An IgE mediated response to an allergen. Could also be a non IgE mediated response such as smoke, or temp.

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40
Q

What is a food allergy

A

An adverse health effect arising from a specific immune response that occurs reproducibly after exposure to a given food

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41
Q

What are the common food allergies in children

A

Eggs, milk, and peanuts. Highest prevalence is in children with moderate to severe atopic dermatitis. (others include shellfish, tree nuts, soy, wheat,)

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42
Q

What are the common food allergies in adults

A

Fish, shellfish, peanuts, tree nuts, soybean, and some fruits

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43
Q

What is the difference between a food allergy and an adverse food reaction

A

Food allergies actually activate the immune system where as adverse reactions usually involve more of the body’s metabolic activities. Only 3-4 % of the adult population actually has a food allergy

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44
Q

What are IgE -mediated food allergies (or mixed IgE)

A
  1. Immediate GI anaphylaxis
  2. eosinophilic esophagitis/gastroenteritis
  3. Oral allergy syndrome
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45
Q

Clinical presentation (time frame) of IgE-mediated food allergies

A
  1. Occur within minutes-2hrs

2. Hives, flushing, facial angioedema, throat itching

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46
Q

Clinical presentation (time frame) of non IgE mediated or mixed disorders for food allergies

A
  1. Delayed onset of more than several hours

2. Similar symptoms as the IgE mediated reactions.

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47
Q

What does the CDC recommend for vaccines in all adults

A
  1. Seasonal influenza
  2. Td every 10 years
  3. Tdap once instead of Td
  4. Varicella
  5. MMR
  6. Other vaccines will be determine by other factors such as age, lifestyle job, etc
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48
Q

What vaccine should not be used in immunocompromised patients

A

Active (live attenuated) vaccines

1. MMR 2. Varicella 3. Zoster

49
Q

Etiology of exanthematous (morbilliform eruption)

A

Caused from ingestion or parenterally administered drug. Adverse hypersensitivity to drugs

50
Q

Clinical presentation of exanthematous

A

Most common type of cutaneous drug reaction.
Bright red macules/papules. Over time lesions form large macules in a sheet like fashion. Diffuse and symmetric distribution over the trunk and extremities. (occur usually one week after drug admin.)
Pruritic

51
Q

Lab findings of exanthematous

A
  1. Peripheral eosinophilia

2. Perivascular lymphocytes and eosinophils

52
Q

Management of exanthematous (morbilliform)

A
  1. Identify offending drug and discontinue.
  2. Oral antihistamine - alleviate pruritus
  3. Glucocorticoids - topical or systemic
53
Q

Patient education of exanthematous

A

Must be aware of the drug hypersensitivity and that other drugs of the same class may cross react. Medical alert bracelet advised

54
Q

Etiology of fixed drug eruption

A

Adverse cutaneous reaction due to an ingested drug. Occurs 30min-8hr. Often caused by tetracyclines, sulfonamides, metronidazole, NSAIDS.

55
Q

Clinical presentation of fixed drug eruption

A

Formation of a solitary (maybe multiples) erythematous patch or plaque. Can be painful or itchy. If sensitive to a drug, the patch will continue to show up in the same spot within hours of ingestion. SPOT ALWAYS COMES BACK IN SAME AREA
seen in mouth, genitalia, face, acral areas

56
Q

Lab tests/findings of fixed drug eruptions

A

Patch test - drug in question can be placed on patch, not very useful though (30%).

57
Q

Management of fixed drug eruptions

A
  1. Withhold offending drug
  2. Treat noneroded lesions with topical steroid
  3. Eroded lesions treat with antimicrobial ointment.
58
Q

Etiology of drug induced hypersensitivity syndrome (AKA DRESS - drug related eosinophilia and system symptoms)

A

Most commonly caused by anti epileptic drugs and sulfonamides. Other drugs are NSAIDS, anti HIV drugs, ABX. Onset is 2-6 weeks after drug is used (onset is how we distinguish it from exanthematous)

59
Q

Clinical presentation of DRESS

A
  1. Fever/malaise
  2. Facial edema
  3. Exfoliative dermatitis
  4. Morbilliform eruption on face, upper trunk, upper ext.
  5. Longer - eruptions become edematous.
    Sometimes hard to differentiate between exanthematous eruptions - look for systemic issues.
    (skin eruption, systemic symptoms, internal organ involvement).
60
Q

Lab findings in DRESS

A
  1. Eosinophilia
  2. Leukocytosis
  3. Signs of hepatitis and interstitial nephritis
  4. order a CBC and LFT
61
Q

Management of DRESS

A
  1. Discontinue drug
  2. Glucosteroids - but may cause rash to recur
  3. Systemic - prednisone if severe reaction (helps prevent organ failure, mostly kidney)
62
Q

Etiology of Steven-Johnson syndrome

A

Caused by ingestion of medication due to an immune-complex hypersensitivity (type III). SATAN - drugs

63
Q

Clinical presentation of steven-johnson syndrome

A
  1. Lesser form of toxic epidermal necrolysis
  2. Burning rash that begins symmetrically on the face and upper torso. Form blisters.
  3. Necrotic tissue near lesions on mucous membrane
  4. Fever/fatigue/sore throat
  5. Shows up on lips and mouth
    DEADLY IF NOT TREATED
64
Q

Lab findings for Steven-Johnson

A

TNF
Interleukin
c-reactive protein
No real test to definitely establish a diagnosis

65
Q

Management of Steven-Johnson

A
  1. Maintain airway
  2. Hemodynamic stability
  3. Treat as a wound/burn care
  4. Oral topical anesthetics
66
Q

Etiology of Toxic epidermal necrolysis (TEN)

A

Caused by ingestion of a drug. But may also be caused by infection, malignancy, and vaccines. (sulfonamides, chloramphenicol, macrocodes, penicillins). SATAN drugs

67
Q

Clinical presentation of TEN

A
  1. Widespread erythema
  2. Necrosis
  3. Bullous detachment of epidermis/mucous membranes
  4. Resp. failure, GI bleeding
    LIFE THREATENING!
68
Q

Lab tests of TEN

A

Analysis of skin lesions. Will see scatter lymphocytic infiltration of the dermis

69
Q

Management of TEN

A
  1. Fluids
  2. Electrolyte balance
  3. Nutritional support
  4. Burn/wound care
70
Q

What vaccines are given to adults over 60 and over 65

A

Zoster - 60years

Pneumococcal polysaccharide, pneumococcal 13 - 65 years

71
Q

What vaccine is given to women between the ages of 19-26

A

HPV

72
Q

What drugs do HIV patients commonly have a cutaneous reaction to

A

Sulfonamides

73
Q

What drug do people with Epstein Barr virus have a reaction to

A

Ampicillin

74
Q

How do you differentiate between SJS and TEN

A

Body surface area. TEN is more than 30% of surface. If less than 10% it is SJS

75
Q

Diagnostic work up of allergic rhinitis

A
  1. HEENT
  2. Conjunctivitis
  3. Otitis media
  4. Turbinate hypertrophy
  5. Eosinophilia blood test, CBC, skin tests
76
Q

What other issues are usually going on in children with food allergies

A

Asthma and atopic dermatitis

77
Q

What is the pathophysiology of a food allergy

A

Helper T cells identify foreign object
Good immune: Th1 cells respond resulting in IgG production
Allergy producing immunity: The Th2 cells results in release of inflammatory mediators that cause allergy symptoms and results in IgE

78
Q

What are the 2 types of food allergy categories

A
  1. IgE mediated - Food induced

2. Non-IgE mediated - typically preservative induced or specific protein induced

79
Q

Etiology of IgE food allergies

A

Direct response to a specific protein on the ingested food

80
Q

Signs/symptoms of IgE mediated food allergy

A
  1. skin - urticaria, rash
  2. Respiratory - anaphylaxis
  3. GI - vomiting, diarrhea
81
Q

What are the 2 IgE mediated food allergies

A
  1. Immediate (GI hypersensitivity and anaphylaxis)

2. Oral allergy syndrome

82
Q

What are the clinical signs of oral allergy syndrome

A
  1. Swelling/redness of lips
  2. Tongue swelling
  3. Local temporary reaction
  4. Not usually systemic
83
Q

What usually causes oral allergy syndrome

A
  1. Contact with raw nuts
  2. Fresh fruits/veggies
  3. Some environmental
  4. Not usually associated with cooked foods
84
Q

What are the 2 mixed IgE/non IgE mediated food allergies

A
  1. Eosinophilic Esophagitis

2. Eosinophilic gastritis

85
Q

Clinical presentation of EoE (eosinophilic esophagitis)

A
  1. Abd pain/cramping
  2. Dysphagia
  3. Food refusal
  4. Chronic vomiting
86
Q

What are the most common causes of EoE

A
  1. Milk*
  2. Wheat
  3. Egg
  4. Soy
  5. Peanut
    In order of most common to least
87
Q

What are non-IgE food allergies caused by

A
  1. other immunologic responses
    - intestinal reaction, vomiting and diarrhea
  2. Proctocolitis
  3. Food protein induced enterocolitis
  4. Celiac disease
88
Q

What is the food that causes food protein induced enterocolitis

A

Milk

89
Q

How do you diagnose a food allergy

A
  1. Medical and diet hx
  2. PE
  3. SPT
  4. allergen specific IgE
  5. Oral food challenge
90
Q

What food allergies are the SPT useful for

A

IgE mediated reactions

91
Q

What food allergies are atopy patch tests good for

A

EoE, FPIES, and atopic dermatitis

92
Q

What food allergies are the allergen specific serum test good for

A

IgE mediated reactions. Reflects presence of IgE but not necessarily a clinical allergy

93
Q

What are examples of food intolerances

A
  1. lactose, sucrose, fructose
  2. caffeine, drugs
  3. toxins
    Usually associated with digestions/absorption issues (metabolic)
94
Q

Etiology of contact dermatitis (2 types)

A
  1. Irritant dermatitis - chemical, cleaning agents

2. Allergic dermatitis - Poison ivy, dyes, medications

95
Q

Clinical presentation of contact dermatitis

A
  1. Irritant - Burning, stinging, itching - 24hrs after exposure
  2. Allergic - Reexposure that has intense pruritus, stinging and pain
96
Q

Physical exam findings of contact dermatitis

A

Irritant is usually found on hands and may spread. Allergic is usually found wherever the pt came into contact with allergen.

97
Q

Etiology of atopic dermatitis

A

Unknown, but usually a genetic component. IgE reaction, T cell dysfunction may play a role

98
Q

Clinical presentation of atopic dermatitis

A
  1. Chronic pruritus - shows up on face mostly in children. On flexural areas in adults
  2. Dry skin
  3. Itch-scratch cycle
  4. May have conjunctivitus or rhinitis
99
Q

PE findings of atopic dermatitis

A

Pruritus on face, trunk, and extremities. Also around flexural surfaces

100
Q

Treatment of contact dermatitis

A
  1. avoid contact
  2. use topical or oral steroids
  3. antihistamines
101
Q

Treatment of atopic dermatitis

A
  1. Stop scratching, will cause secondary lesions with possible infection
  2. Steroids
  3. Antihistamines
  4. Phototherapy
102
Q

Etiology of lichen simplex

A

Results from repetitive rubbing and scratching

103
Q

Clinical presentation of lichen simplex

A
  1. Solid plaque of lichenification
  2. Skin is thick
  3. Possible excoriations
104
Q

Treatment of lichen simplex

A
  1. Stop rubbing
  2. Occlusive bandages
  3. Topical glucocorticoids
105
Q

Etiology of nummular (discoid) eczema

A

Unknown, possible a sensitivity reaction. Sometimes associated with dry skin and eczema

106
Q

Clinical presentation of nummular eczema

A

Coin shaped plaques made up of small papules and vesicles on a red base.
May be itchy and burn

107
Q

Treatment of nummular eczema

A
  1. Moisturize
  2. Avoid harsh soaps
  3. Topical steroids
  4. Tar ointment
108
Q

Etiology of dishidrotic eczema

A

Special vesicular type of hand and foot dermatitis

109
Q

Clinical presentation of dishidrotic eczema

A

Sudden onset of deep pruritic clear tapioca like vesicles.

Itching and pain

110
Q

Treatment of dishidrotic eczema

A
  1. Topical high potency corticosteroids

2. Possible oral steroids

111
Q

What is the mechanism (how does it work) of immunotherapy

A

Decreases the IgE levels and results in an increase in allergen specific IgG levels that inhibit mast cell degranulation

112
Q

Who is an appropriate patient to put on immunotherapy

A
  1. Poor response to other drugs
  2. Symptoms of bronchial asthma
  3. Bothersome side effects with commonly used drugs
  4. Can be considered in patients with new onset of allergic asthma
113
Q

How are immunotherapy drugs administered

A

Incremental dosing over 10-24 weeks and maintenance injections from 3-5 years

114
Q

Spectrum of allergic reaction to vaccines

A

Mild: local at injection site
Severe: immediate (anaphylaxis) within 5-30 minutes

115
Q

Causes of allergic reactions in vaccines

A
  1. Gelatin
  2. Egg protein
  3. Antimicrobial agents (neomycin, plymyxin)
  4. Yeast
  5. Latex
116
Q

Common reactions to vaccines

A
  1. immediate is the most common - itching, lightheadedness, syncope, nasal congestion, throat closure
  2. Delayed reaction less common - fever, local swelling, pruritus
117
Q

Idiosyncratic drug reactions

A

These reactions are usually due to hereditary enzyme deficiency. They can either be IgE or non-IgE and are highly unpredictable but do not occur in many people. Can be severe though. One example is DRESS - drug induced hypersensitivity syndrome.

118
Q

Example of IgE drug mediated reaction

A

Penicillin

119
Q

Example of IgG/IgM drug mediated reaction

A

ABX, immunoglobulins

AII week 1 (4 decks)

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