1
Q
What aspect of the immune system requires no prior exposure to pathogens?
A
Innate Immunity
2
Q
What aspect of our immune system is rapid, non-specific, and does not provide long-lasting protection?
A
Innate Immunity
3
Q
What are the non-cellular components of innate immunity?
A
- Epithelial and mucous membranes
- Complement system proteins
- Acute phase proteins
4
Q
What are the cellular components of the innate immunity system?
A
- Neutrophils
- Macrophages
- Monocytes
- NK cells
5
Q
What cell (of the innate immunity response) responds the fastest to infection?
A
Neutrophils
6
Q
What cell (of the innate immunity response) provides a slower but more prolonged response to infection?
A
Macrophages
7
Q
What is the Complement System?
A
Over 30 plasma and cell surface proteins that complements both innate and adaptive immunologic systems.
8
Q
What does the Complement system do to enhance the adaptive and innate immunologic systems?
A
- Augments phagocytes and antibodies
- Marks pathogens for permanent destruction
9
Q
Where are the proteins for the Complement system produced?
A
Liver
10
Q
What activates the complement system?
A
Infection of course.
C1 and C3 (Complement proteins 1 & 3).
11
Q
What is the most numerous WBC?
A
Neutrophils
12
Q
What are the characteristics and actions of neutrophils?
A
- Migrate rapidly to bacterial infections
- Release cytokines to phagocytize
- ½ life of 6 hours
- Sensitive to acidic infection environments
- Become purulent exudate
13
Q
What type of immune cell is the largest blood cell and circulates to specific tissue areas to differentiate into macrophages?
A
Monocytes
14
Q
What are the names of monocytes that have circulated to following areas:
- Epidermis
- Liver
- Lungs
- CNS
A
- Epidermis → Langerhans
- Liver → Kupffer
- Lung → Alveolar cells
- CNS → Microglia
15
Q
What are the pertinent characteristics of monocytes/macrophages?
A
- Mobilize after neutrophils
- Phagocytic destruction via NO & cytokines
- Persist at site in chronic infections
16
Q
What is the least common blood granulocyte?
A
Basophils
17
Q
What cells reside in connective tissue close to blood vessels?
A
Mast Cells
18
Q
What are the characteristics/actions of basophils/mast cells?
A
- Express high affinity for IgE
- Initiate hypersensitivity (produce histamine, leukotrienes, PG’s, and cytokines)
- Stimulate smooth muscle contraction
19
Q
What cells play a major role in allergies, asthma, and eczema?
A
Basophils and Mast cells
20
Q
What cell type is classified by the following characteristics:
- Heavily concentrated in GI mucosa
- Protects against parasites
- Degrade mast cell inflammation
A
Eosinophils
21
Q
What characteristics does Adaptive Immunity possess?
A
- Present only in Vertebrates
- Delayed onset of action
- Capable of memory and specific antigen response
22
Q
What type of cells do adaptive immunity cells originate from?
A
Hematopoietic stem cell
23
Q
What is the humoral component of the Adaptive Immunity system?
What does this component do?
A
B cells → produce antibodies
24
Q
What are the cellular components of the adaptive immunity system?
A
Helper T-cells
Cytotoxic T-cells
25
Where do T-cells originate? Where do they mature?
T-cells originate in the bone marrow and mature in the Thymus.
26
What are the general characteristics of T-cells?
- Produce interferon and interleukins
- Activate IgE
- Role in chronic inflammation
27
What is the primary example of passive immunity?
Maternal IgA antibodies from breast milk
28
What is the primary example of active immunity?
Vaccines
29
Is neutropenia an example of excessive or inadequate immune response?
Inadequate
30
What is required for hypersensitivity development?
Prior sensitization (grass, latex, nuts, etc)
31
What is hypersensitivity?
Foreign antigen response caused by altered T-cell and antibody response
32
What is the most common source of hypersensitivity?
Drugs (ABX, PPIs, etc.)
33
What are examples of a Type I allergic response (aka immediate hypersensitivity)?
Anaphylaxis, Asthma, Angioedema, Conjuctivitis, Dermatitis
34
What occurs during a Type I Allergic Response?
- 1st exposure: T-Cells stimulate B cells to produce IgE
- 2ⁿᵈ exposure: Released Ca⁺⁺ → histamine, inflammatory mediators, heparin.
(Histamine triggers: bronchostriction, permeability, vasodilation)
35
What are common drugs used to prevent the histamine effects of Type I allergic responses?
- Antihistamines
- Cromolyn Na⁺
- Bronchodilators
- COX Inhibitors
36
What is another name for Type II Allergic Responses?
What mediates these types of responses?
- Cytotoxic Hypersensitivity
- Mediated by **IgG, IgM, and Complement system** → B-cells → antibodies.
37
What are examples of Type II Allergic Responses?
- Hemolytic Anemia
- Myasthenia Gravis
- Transfusion Reactions
38
What is the treatment for Type II Allergic Responses?
- Anti-inflammatories
- Immunosuppressants
39
What is another name for Type III Allergic Response?
Immune Complex Hypersensitivity
40
What occurs with Type III Allergic Response?
Failure of immune system to eliminate antibody-antigen complex.
41
Where are the antibody-antigen complexes deposited in immune complex hypersensitivity?
Joints, kidneys, skin, eyes
42
What antibodies mediate Type III Allergic Responses?
IgG and IgM
43
What are examples of Type III Allergic Responses?
SLE and Rheumatoid arthritis
44
What are examples of Type IV Allergic Responses?
- Contact Dermatitis
- Tuberculosis
- Stevens-Johnson Syndrome
45
What is a Type IV Allergic Response?
T-lymphocyte and monocyte/macrophage mediated response that **does not involve antibodies**.
46
What are the most common symptoms with Type IV Allergic Responses?
Cutaneous symptoms
47
What rhythm occurs with untreated anaphylaxis?
PEA
48
What causes the loss in BP noted with anaphylaxis?
Vasodilation from NO release
49
What is the pathophysiology of anaphylaxis?
50
What is Biphasic anaphylaxis?
Secondary anaphylactic episode occurring 8 - 72 hours later.
51
What are risk factors for a secondary anaphylactic episode?
- Severe initial response
- Initial response requiring multiple epi doses
52
What are risk factors for perioperative anaphylaxis?
- Asthma
- Female
- Prolonged Anesthetic
- Multiple past surgeries
- Presence of other allergic conditions
53
What lab can verify mast cell activation and release?
Plasma Tryptase
54
Plasma histamine concentration should be at baseline within _____ minutes of treatment.
60 minutes
55
When is anaphylactic response skin testing typically done after an episode?
Wheal and flare response 6 weeks after initial reaction.
56
What is the treatment for anaphylaxis?
- Call for help
- Stop blood, drugs, colloids
- 100% O₂
- Epi
- Fluids
57
What is the epinephrine dose for adult anaphylaxis?
10 mcg - 1000mcg IVP q 1-2 min
58
What is the epinephrine dose for child anaphylaxis?
1-10 mcg/kg IVP q 1-2 min
59
If a patient experiencing anaphylaxis is resistant to epi, what should be given?
Vasopressin or Methylene blue
*These will inhibit NO production and thus counteract vasodilation*.
60
What is the crystalloid dosage for anaphylaxis?
10 - 25 mL/kg over 20 min
61
What is the colloid dosage for anaphylaxis?
10 mL/kg over 20 min
62
Why is epinephrine the drug of choice for anaphylaxis?
- ↓ degranulation of mast cells & basophils → reduced vasodilation
- α1 = Increased blood pressure
- β1 = Inotropy & chronotropy
- β2 = Bronchodilation
63
What drug classes are secondary treatments for anaphylaxis?
- Bronchodilators
- Antihistamines
- Corticosteroids
64
What are the antihistamines (and dosages) used as secondary treatments for anaphylaxis?
- H1 → Diphenhydramine 0.5 - 1 mg/kg IV
- H2 → Ranitidine 50 mg IV
65
What are the corticosteroids (and dosages) used as secondary treatments for adult anaphylaxis?
- Hydrocortisone 250 mg IV
- Methylprednisolone 80 mg IV
66
What are the corticosteroids (and dosages) used as secondary treatments for pediatric anaphylaxis?
- Hydrocortisone 50-100 mg IV
- Methylprednisolone 2 mg/kg IV
67
What causes Graves disease?
Autoantibodies to TSH receptor
68
What is affected by the immune response characteristic of SLE?
RBCs, WBCs, nucleic acids, platelets, coag proteins
69
What is/are the cause(s) of hereditary angioedema?
C1 Esterase inhibitor deficiency/dysfunction → excessive bradykinin production.
70
What factors can cause C1 esterase problems?
- Menses
- Trauma
- Infection
- Stress
- Oral contraceptives
71
What typically limits the production of excessive bradykinin?
C1
*C1 limits kallikrein and Factor XIIa*.
72
What occurs anatomically with excessive bradykinin?
- Laryngeal swelling
- Vasodilation
73
What dose of antihistamine should be used for hereditary angioedema?
Trick question. Hereditary Angioedema = excessive bradykinin and is unaffected by antihistamines.
74
What body parts are typically effected by hereditary angioedema?
Legs, hands, face, upper resp tract
75
What is the typical cause of acquired angioedema?
- ACE Inhibitors
76
What symptoms are conspicuously absent with acquired angioedema?
No Urticaria or Pruritus
77
What is responsible for the breakdown of bradykinin?
ACE
*Thus ACE inhibitors = ↑ bradykinin = angioedema*.
78
What are the treatments for Angioedema?
- Airway maintenance
- FFP
- C1 Inhibitor concentrate
- Epinephrine
- Antihistamines
- Glucocorticoids?
79
What cells are destroyed by the HIV virus?
Monocytes/Macrophages and T-cells
80
How long does seroconversion take after inoculation with the HIV virus?
2-3 weeks
81
What are the initial signs and symptoms of HIV conversion to AIDS?
Weight loss and failure to thrive
82
How is HIV/AIDS diagnosed?
- ELISA: 4-8 weeks after infection
- Viral Load
- CD4/Helper T lymphocytes < 200k
- HAART agent sensitivity
83
Inhibition of the liver's ________ has huge implications for anesthetic delivery in HIV/AIDS patients.
CYP 450's
84
What s/s characterize scleroderma?
- Inflammation
- Vascular Sclerosis
- Fibrosis of skin/viscera
85
At what age does scleroderma typically occur?
What gender is typically affected?
- 20-40
- Females
86
What GI symptoms of scleroderma are particularly pertinent to anesthesia?
- GI Tract Hypomotility
- ↓ LES tone
87
______ fibrosis and ______ artery stenosis are prominent considerations for anesthesia in scleroderma patients.
Pulmonary fibrosis and renal artery stenosis
88
What are the overall anesthesia implications of scleroderma?
- Arterial catheter issues
- Contracted intravascular volume
- Aspiration risk
- Limited neck mobility
- ↓ pulmonary compliance
89
What do inhalation agents do the immune system?
- Suppress NK cells
- Induce apoptosis of T-cells
- Impair phagocytes
*Unclear effects on tumor cells*.
90
This benzodiazepine, ________, decreases the migration of neutrophils.
Midazolam
91
This induction agent, _______, will depress natural killer cell activity.
Ketamine
92
This induction agent, ________, decreases cytokines but promotes NK cells.
Propofol
93
What drug class will suppress NK cells?
Opioids
*Particularly morphine and fentanyl*.
94
What cell type plays the greatest role in chronic inflammation?
T-Cells
95
What cell type activates IgE and produces interleukins and interferons?
T-Cells
Decks in class (23)
# Cards
-
X-Rays (Exam I)53
-
Test 1: Chest X-Rays (Andy's Cards)127
-
Test 1: Radiology/ Laser Safety (Andy's Cards)68
-
Test 1: Burns (Andy's Cards)125
-
Cardiac Monitoring (Exam I)53
-
Basic & Advanced EKG (Exam I) (Assessment Review)89
-
Geriatrics (Exam II)60
-
HAI & Antibiotics (Exam II)82
-
SCIP & ERAS (Exam II)44
-
PACU & Complications (Exam II)100
-
Acute Pain & Opioid-Free Analgesia (Exam II)128
-
Immune Dysfunction (Exam III)95
-
Obesity (Exam III)60
-
PONV (Exam III)57
-
Oncology and Chemotherapy (Exam III) Andy's Cards113
-
Missed Exam II Questions11
-
Maverick Modules (1-4) Regional Block Basics7
-
Maverick Modules (5-6) Drugs & Toxicity Basics29
-
Maverick Modules (7-9) ISB, Femoral, & Lateral Popliteal Sciatic Blocks40
-
Maverick Modules (10 - 16) Ultrasound Basics26
-
Maverick Modules (17 - 19) Ultrasound SCB, ISB, & ANB26
-
Maverick Modules (20 - 22) Ultrasound FNB, ACB, PPB18
-
Maverick Modules (23-26) PENG, LFCB, PSB, & Post-Op21
