Exam 3 - Immune Dysfunction (Grayson's) Flashcards
Select 2. Innate immunity is characterized by being:
A. present only in vertebrates
B. capable of memory and having a specific antigen response
C. having a delayed onset
D. rapid and non-specific
E. requiring no prior exposure
D. rapid and non-specific
E. requiring no prior exposure
Select 2. Innate immunity has:
A. no memory
B. specific antigen response
C. memory activation thru vaccines
D. a response that is always identical
A. no memory
D. a response that is always identical
Non-cellular elements of innate immunity include: select 3
A. macrophages
B. complement
C. acute phase proteins
D. epithelial and mucous membranes
E. B cells and T cells
F. neutrophils
B. complement
C. acute phase proteins
D. epithelial and mucous membranes
Which cellular element of innate immunity has the fastest response?
A. neutrophils
B. macrophages
C. monocytes
D. natural killer cells
A. neutrophils
Which cellular element of innate immunity has a slower but more prolonged response?
A. neutrophils
B. macrophages
C. monocytes
D. natural killer cells
B. macrophages
Complement proteins complement the role of immune cells as part of both innate and adaptive immunity. What do they do specifically?
A. migrate rapidly in bacterial infections and release cytokines
B. protect against parasites
C. augment phagocytes and antibodies by marking pathogens for permanent destruction
D. produce nitric oxide to cause vasodilation
C. augment phagocytes and antibodies by marking pathogens for permanent destruction
Complement proteins are 30+ plasma and cell surface proteins that are produced in the liver. What are they activated by?
A. C1 or C3
B. RBCs
C. Kupffer cells
D. histamine
A. C1 or C3
aka complement-1 or complement-3
Neutrophils are the most numerous of WBCs. Their job is to: select 2.
A. produce NO
B. release cytokines and phagocytize
C. stimulate smooth muscle contraction
D. migrate rapidly in bacterial infections
E. degrade mast cell inflammation
B. release cytokines and phagocytize
D. migrate rapidly in bacterial infections
What is the half-life of neutrophils?
A. 2 hrs
B. 6 hrs
C. 12 hrs
D. 24 hrs
B. 6 hrs - so don’t really last that long b/c sensitive to acidic environments of infection
they breakdown and become purulent exudate (pus)!
This innate immune cell is the largest blood cell and mobilizes just after neutrophils.
A. basophils
B. mast cells
C. monocytes
D. eosinophils
C. Monocytes - which are called macrophages when they circulate to tissue specific areas.
What are the names of monocytes that have circulated to following areas:
- Epidermis
- Liver
- Lungs
- CNS
- Epidermis → Langerhans
- Liver → Kupffer
- Lung → Alveolar cells
- CNS → Microglia
Monocytes/macrophages produce what 2 substances that cause vasodilation and help other immune cells get there?
A. nitric oxide
B. histamine
C. leukotrienes
D. cytokines
A. NO
D. cytokines
unlike neutrophils, monocytes/macrophages persist at sites of chronic infection
What is the least common blood granulocyte?
A. mast cells
B. basophils
C. eosinophils
D. neutrophils
B. basophils
What cells reside in connective tissue close to blood vessels?
A. mast cells
B. basophils
C. eosinophils
D. neutrophils
A. mast cells
Basophils and mast cells express high affinity receptors for IgE. This makes them initiators of hypersensitivity which causes release of what:
A. histamine
B. leukotrienes
C. cytokines
D. prostaglandins
E. interferon
F. all of the above
G. all of the above except E
G. all of the above except E.
so basophils and mast cells cause release of: histamine, leukotrienes, cytokines, and prostaglandins
What cells stimulate smooth muscle cxn and play a major role in allergies, asthma, and eczema?
A. eosinophils
B. macrophages
C. mast cells and basophils
D. helper T cells
C. Mast cells and basophils
b/c of their release of histamine, leukotrienes, cytokines, and PGs!
Eosinophils are heavily concentrated in GI mucosa. They are helpful because they: select 2.
A. stimulate smooth muscle contraction
B. produce antibodies
C. protect against parasites
D. degrade mast cell inflammation
C. protect against parasites
D. degrade mast cell inflammation
Adaptive immunity is present only in vertebrates. It also has: select 2.
A. the quickest onset of action
B. memory capability and a specific antigen response
C. a delayed onset of action
D. no memory
B. memory capability and specific antigen response
C. Delayed onset of action
VACCINES can also activate this memory!!
Which cells make up the humoral component of adaptive immunity that produce antibodies?
A. T cells
B. B cells
C. eosinophils
D. basophils
B. B cells = produce antibodies
Antibodies bind to foreign proteins of bacteria, viruses, and tumors!
select all that apply
The cellular components of adaptive immunity include:
A. mast cells
B. cytotoxic t-cells
C. b cells
D. helper t-cells
B. cytotoxic T-cells
D. helper T-cells
T-cells originate in bone marrow and they mature in the:
A. spleen
B. thymus
C. liver
D. thyroid
B. thymus - so ppl with a thymectomy do not have this immune response from T cells!
What do T-cells produce that play a role in chronic inflammation and infection response? select 2.
A. interferon
B. interleukin
C. leukotrienes
D. prostaglandins
A. interferon
B. interleukin
also activate IgE!!!
What is an example of passive immunity? select 2.
A. recombinant vaccines
B. repeat exposures to pathogens
C. IV immunoglobulin therapy
D. maternal IgA antibodies via breast milk
C. IV immunoglobulin therapy
D. Maternal IgA antibodies from breast milk
The primary example of active immunity is:
Vaccines
What is an example of an inadequate immune response?
A. neutropenia
B. asthma
C. seasonal allergies
D. eczema
A. neutropenia
What is an example of excessive or exaggerated (hypersensitivity) immune response?
A. systemic lupus erythematosus
B. asthma
C. rheumatoid arthritis
D. neutropenia
B. asthma
What is required for a hypersensitivity reaction to occur?
A. being born preterm
B. a prior sensitization
C. new medications
D. moving to a new city
B. Prior sensitization (grass, latex, gluten, nuts, medications, etc)
What is the most common source of hypersensitivity rxn?
A. latex
B. nuts
C. grass
D. medications
D. meds - especially muscle relaxers (w/ rocuronium being number #1!)
but also NSAIDs, antibiotics, PPIs
What are examples of a Type I allergic response (aka immediate hypersensitivity)? select 2.
A. angioedema
B. anaphylaxis
C. hemolytic anemia
D. transfusion reaction
A. Angioedema
B. Anaphylaxis
Describe the events that occur during a Type I Allergic Response. (1st exposure and 2nd exposure..)
- 1st exposure: T-Cells stimulate B cells to produce IgE
- 2ⁿᵈ exposure: Released Ca⁺⁺ → histamine, inflammatory mediators, heparin.
(Histamine triggers: bronchostriction, permeability, vasodilation)
select all that apply:
What are common drugs used to prevent the histamine effects of Type I allergic responses?
A. diphenhydramine
B. immunosuppressive agents
C. bronchodilators
D. cromolyn sodium
E. dexamethasone
F. COX pathway inhibitors
A. diphenhydramine (Benadryl) = antihistamines!
C. bronchodilators
D. cromolyn sodium
F. COX pathway inhibitors
What mediates a Type II Allergic Response aka “cytotoxic hypersensitivity?”
A. failure of the immune system to eliminate antibody-antigen complex
B. IgG, IgM and complement
C. IgE
D. monocyte/macrophages
B. Mediated by IgG, IgM, and Complement system → activate B-cells → to produce antibodies.
What are examples of Type II Allergic Responses? select 3.
A. rheumatoid arthritis
B. conjunctivitis
C. hemolytic anemia
D. myasthenia gravis
E. SLE
F. transfusion reactions
C. Hemolytic Anemia
D. Myasthenia Gravis
F. Transfusion Reactions
What is the treatment for Type II Allergic Responses?
- Anti-inflammatories
- Immunosuppressants
What occurs with Type III Allergic Response aka “immune complex hypersensitivity?”
A. IgG, IgM and complement activate B cells to make antibodies
B. failure of the immune system to eliminate antibody-antigen complex
C. IgE antibodies are produced
D. usually just cutaneous symptoms
B. failure of the immune system to eliminate antibody-antigen complex - these complexes get deposited in joints, kidneys, skin, eyes
technically also mediated by IgG and IgM1
What are examples of Type III Allergic Responses? select 2.
A. lupus
B. myasthenic syndrome
C. rheumatoid arthritis
D. angioedema
A. SLE
C. Rheumatoid arthritis
treat with anti-inflammatories and maybe immunosuppressives
T/F: Type IV allergic responses do not involve antibodies.
True. Type IV are T lymphocyte and monocyte/macrophage mediated and do not involve antibodies.
Cutaneous symptoms are most common with Type IV allergic responses. What are examples?
A. angioedema
B. contact dermatitis
C. Stevens-Johnson Syndrome
D. conjunctivitis
B. contact dermatitis
C. Stevens-Johnson Syndrome
and: Tuberculosis
What occurs with untreated anaphylaxis?
PEA
What is the pathophysiology of anaphylaxis?
flip for diagram
What is Biphasic anaphylaxis?
Secondary anaphylactic episode occurring 8 - 72 hours later… without second exposure.
What are risk factors for a secondary anaphylactic episode?
- Severe initial response
- Initial response requiring multiple epi doses
What are risk factors for perioperative anaphylaxis? select 3.
A. longer duration of anesthesia
B. males
C. HTN and diabetes
D. multiple past surgeries
E. family hx of MH
F. asthma
A. longer duration of anesthesia
D. multiple past surgeries
F. asthma
also:
- females (not teens)
- presence of other allergic conditions
What laboratory value can verify mast cell activation and release?
A. plasma tryptase
B. positive TB test
C. plasma histamine
D. wheel and flare response
A. Plasma Tryptase concentration - 1-2 hrs after anaphylaxis
Plasma histamine concentration should be at baseline within ____ minutes of treatment.
A. 15
B. 30
C. 60
D. 180
C. 60 minutes
Skin testing is done 6 weeks after anaphylactic reaction. What response determines a positive result?
Wheal and flare response
What is the treatment for anaphylaxis?
- Call for help
- Stop administration of blood, drugs, colloids
- 100% O₂
- Epi = FIRST LINE DRUG!!!!
- Fluids
What is the epinephrine dose for adult anaphylaxis?
10 mcg - 1mg IVP q 1-2 min
What is the epinephrine dose for child anaphylaxis?
1-10 mcg/kg IVP q 1-2 min
If a patient experiencing anaphylaxis is resistant to epi, what should be given? select 2.
A. norepinephrine
B. vasopressin
C. benadryl
D. methylene blue
E. dopamine
B. Vasopressin and/or
D. Methylene blue
These will inhibit NO production and thus counteract vasodilation!
What is the crystalloid (NS) dosage for anaphylaxis?
10 - 25 mL/kg over 20 min; repeat PRN
What is the colloid dosage for anaphylaxis?
10 mL/kg over 20 min; repeat PRN
Why is epinephrine the drug of choice for anaphylaxis?
- ↓ degranulation of mast cells & basophils (vasodilation/hypotension)
- α1 agonist = increases blood pressure
- β1 agonist = positive Inotropy & chronotropy
- β2 agonist = Bronchodilation
What drug classes are secondary treatments for anaphylaxis?
- Bronchodilators (SABA2 like albuterol!)
- Antihistamines (h1 and h2 blockers)
- Corticosteroids (hydrocortisone or methylprednisolone)
What are the antihistamines (and dosages) used as secondary treatments for anaphylaxis?
- H1 blocker → Diphenhydramine (Benadryl) 0.5 - 1 mg/kg IV
- H2 blocker → Ranitidine (Zantac) 50 mg IV
What are the corticosteroids (and dosages) used as secondary treatments for adult anaphylaxis?
- Hydrocortisone 250 mg IV
- Methylprednisolone 80 mg IV
What are the corticosteroids (and dosages) used as secondary treatments for pediatric anaphylaxis?
- Hydrocortisone 50-100 mg IV
- Methylprednisolone 2 mg/kg IV
What causes Graves disease?
Autoantibodies to TSH receptor
What is affected by the immune response characteristic of SLE?
RBCs, WBCs, nucleic acids, platelets, coag proteins
What is/are the cause(s) of hereditary angioedema?
C1 Esterase inhibitor deficiency/dysfunction → excessive bradykinin production.
What factors can trigger hereditary angioedema?
- Menses
- Trauma
- Infection
- Stress
- Oral contraceptives
What typically limits the production of excessive bradykinin?
C1
C1 limits kallikrein and Factor XIIa.
This excessive bradykinin in hereditary angioedema causes what 2 things?
- Laryngeal swelling
- Vasodilation
T/F: Treatment of hereditary angioedema involves some form of antihistamine.
FALSE. Hereditary angioedema is NOT responsive to antihistamines!
What body parts are typically affected by hereditary angioedema?
Legs, hands, face, upper resp tract
What is the typical cause of acquired angioedema?
- ACE Inhibitors
What symptoms are conspicuously absent with acquired angioedema?
No Urticaria or Pruritus
What is responsible for the breakdown of bradykinin?
ACE
Thus ACE inhibitors = ↑ bradykinin = angioedema.
What are the treatments for Angioedema?
- Airway maintenance - tracheal intubation immediately!
- FFP
- C1 Inhibitor concentrate
- Epinephrine
- Antihistamines
- Glucocorticoids?
What cells are destroyed by the HIV virus?
Monocytes/Macrophages and T-cells
How long does seroconversion take after inoculation with the HIV virus?
2-3 weeks
What are the initial signs and symptoms of HIV conversion to AIDS?
Weight loss and failure to thrive
How is HIV/AIDS diagnosed?
- ELISA: 4-8 weeks after infection
- Viral Load
- CD4/Helper T lymphocytes < 200k
- HAART agent sensitivity
Inhibition of the liver’s ________ has huge implications for anesthetic delivery in HIV/AIDS patients.
CYP 450’s
What s/s characterize scleroderma?
- Inflammation
- Vascular Sclerosis
- Fibrosis of skin/viscera
At what age does scleroderma typically occur?
What gender is typically affected?
- 20-40
- Females
What GI symptoms of scleroderma are particularly pertinent to anesthesia?
- GI Tract Hypomotility
- ↓ LES tone
makes them higher risk for aspiration! maybe need to RSI them?
____ fibrosis and ____ artery stenosis are prominent considerations for anesthesia in scleroderma patients.
Pulmonary fibrosis and renal artery stenosis
What are the overall anesthesia implications of scleroderma?
- Arterial catheter issues
- Contracted intravascular volume
- Aspiration risk
- Limited neck mobility
- ↓ pulmonary compliance
What do inhalation agents do the immune system?
- Suppress NK cells
- Induce apoptosis of T-cells
- Impair phagocytes
Unclear effects on tumor cells.
This benzodiazepine, ____, decreases the migration of neutrophils.
Midazolam
This induction agent, ____, will depress natural killer cell activity.
Ketamine
This induction agent, ____, decreases cytokines but promotes NK cells.
Propofol
What drug class will suppress NK cells?
Opioids
Particularly morphine and fentanyl.
