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JW: Principles II > Immune Dysfunction (Exam III) > Flashcards

Immune Dysfunction (Exam III) Flashcards

1
Q

What aspect of the immune system requires no prior exposure to pathogens?

A

Innate Immunity

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2
Q

What aspect of our immune system is rapid, non-specific, and does not provide long-lasting protection?

A

Innate Immunity

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3
Q

What are the non-cellular components of innate immunity?

A
  • Epithelial and mucous membranes
  • Complement system proteins
  • Acute phase proteins
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4
Q

What are the cellular components of the innate immunity system?

A
  • Neutrophils
  • Macrophages
  • Monocytes
  • NK cells
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5
Q

What cell (of the innate immunity response) responds the fastest to infection?

A

Neutrophils

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6
Q

What cell (of the innate immunity response) provides a slower but more prolonged response to infection?

A

Macrophages

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7
Q

What is the Complement System?

A

Over 30 plasma and cell surface proteins that complements both innate and adaptive immunologic systems.

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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
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9
Q

Where are the proteins for the Complement system produced?

A

Liver

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10
Q

What activates the complement system?

A

Infection of course.

C1 and C3 (Complement proteins 1 & 3).

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11
Q

What is the most numerous WBC?

A

Neutrophils

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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
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13
Q

What type of immune cell is the largest blood cell and circulates to specific tissue areas to differentiate into macrophages?

A

Monocytes

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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
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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
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16
Q

What is the least common blood granulocyte?

A

Basophils

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17
Q

What cells reside in connective tissue close to blood vessels?

A

Mast Cells

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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
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19
Q

What cells play a major role in allergies, asthma, and eczema?

A

Basophils and Mast cells

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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

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21
Q

What characteristics does Adaptive Immunity possess?

A
  • Present only in Vertebrates
  • Delayed onset of action
  • Capable of memory and specific antigen response
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22
Q

What type of cells do adaptive immunity cells originate from?

A

Hematopoietic stem cell

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23
Q

What is the humoral component of the Adaptive Immunity system?
What does this component do?

A

B cells → produce antibodies

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24
Q

What are the cellular components of the adaptive immunity system?

A

Helper T-cells
Cytotoxic T-cells

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25
Q

Where do T-cells originate? Where do they mature?

A

T-cells originate in the bone marrow and mature in the Thymus.

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26
Q

What are the general characteristics of T-cells?

A
  • Produce interferon and interleukins
  • Activate IgE
  • Role in chronic inflammation
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27
Q

What is the primary example of passive immunity?

A

Maternal IgA antibodies from breast milk

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28
Q

What is the primary example of active immunity?

A

Vaccines

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29
Q

Is neutropenia an example of excessive or inadequate immune response?

A

Inadequate

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30
Q

What is required for hypersensitivity development?

A

Prior sensitization (grass, latex, nuts, etc)

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31
Q

What is hypersensitivity?

A

Foreign antigen response caused by altered T-cell and antibody response

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32
Q

What is the most common source of hypersensitivity?

A

Drugs (ABX, PPIs, etc.)

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33
Q

What are examples of a Type I allergic response (aka immediate hypersensitivity)?

A

Anaphylaxis, Asthma, Angioedema, Conjuctivitis, Dermatitis

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34
Q

What occurs during a Type I Allergic Response?

A
  • 1st exposure: T-Cells stimulate B cells to produce IgE
  • 2ⁿᵈ exposure: Released Ca⁺⁺ → histamine, inflammatory mediators, heparin.

(Histamine triggers: bronchostriction, permeability, vasodilation)

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35
Q

What are common drugs used to prevent the histamine effects of Type I allergic responses?

A
  • Antihistamines
  • Cromolyn Na⁺
  • Bronchodilators
  • COX Inhibitors
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36
Q

What is another name for Type II Allergic Responses?
What mediates these types of responses?

A
  • Cytotoxic Hypersensitivity
  • Mediated by IgG, IgM, and Complement system → B-cells → antibodies.
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37
Q

What are examples of Type II Allergic Responses?

A
  • Hemolytic Anemia
  • Myasthenia Gravis
  • Transfusion Reactions
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38
Q

What is the treatment for Type II Allergic Responses?

A
  • Anti-inflammatories
  • Immunosuppressants
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39
Q

What is another name for Type III Allergic Response?

A

Immune Complex Hypersensitivity

40
Q

What occurs with Type III Allergic Response?

A

Failure of immune system to eliminate antibody-antigen complex.

41
Q

Where are the antibody-antigen complexes deposited in immune complex hypersensitivity?

A

Joints, kidneys, skin, eyes

42
Q

What antibodies mediate Type III Allergic Responses?

A

IgG and IgM

43
Q

What are examples of Type III Allergic Responses?

A

SLE and Rheumatoid arthritis

44
Q

What are examples of Type IV Allergic Responses?

A
  • Contact Dermatitis
  • Tuberculosis
  • Stevens-Johnson Syndrome
45
Q

What is a Type IV Allergic Response?

A

T-lymphocyte and monocyte/macrophage mediated response that does not involve antibodies.

46
Q

What are the most common symptoms with Type IV Allergic Responses?

A

Cutaneous symptoms

47
Q

What rhythm occurs with untreated anaphylaxis?

A

PEA

48
Q

What causes the loss in BP noted with anaphylaxis?

A

Vasodilation from NO release

49
Q

What is the pathophysiology of anaphylaxis?

A
50
Q

What is Biphasic anaphylaxis?

A

Secondary anaphylactic episode occurring 8 - 72 hours later.

51
Q

What are risk factors for a secondary anaphylactic episode?

A
  • Severe initial response
  • Initial response requiring multiple epi doses
52
Q

What are risk factors for perioperative anaphylaxis?

A
  • Asthma
  • Female
  • Prolonged Anesthetic
  • Multiple past surgeries
  • Presence of other allergic conditions
53
Q

What lab can verify mast cell activation and release?

A

Plasma Tryptase

54
Q

Plasma histamine concentration should be at baseline within _____ minutes of treatment.

A

60 minutes

55
Q

When is anaphylactic response skin testing typically done after an episode?

A

Wheal and flare response 6 weeks after initial reaction.

56
Q

What is the treatment for anaphylaxis?

A
  • Call for help
  • Stop blood, drugs, colloids
  • 100% O₂
  • Epi
  • Fluids
57
Q

What is the epinephrine dose for adult anaphylaxis?

A

10 mcg - 1000mcg IVP q 1-2 min

58
Q

What is the epinephrine dose for child anaphylaxis?

A

1-10 mcg/kg IVP q 1-2 min

59
Q

If a patient experiencing anaphylaxis is resistant to epi, what should be given?

A

Vasopressin or Methylene blue

These will inhibit NO production and thus counteract vasodilation.

60
Q

What is the crystalloid dosage for anaphylaxis?

A

10 - 25 mL/kg over 20 min

61
Q

What is the colloid dosage for anaphylaxis?

A

10 mL/kg over 20 min

62
Q

Why is epinephrine the drug of choice for anaphylaxis?

A
  • ↓ degranulation of mast cells & basophils → reduced vasodilation
  • α1 = Increased blood pressure
  • β1 = Inotropy & chronotropy
  • β2 = Bronchodilation
63
Q

What drug classes are secondary treatments for anaphylaxis?

A
  • Bronchodilators
  • Antihistamines
  • Corticosteroids
64
Q

What are the antihistamines (and dosages) used as secondary treatments for anaphylaxis?

A
  • H1 → Diphenhydramine 0.5 - 1 mg/kg IV
  • H2 → Ranitidine 50 mg IV
65
Q

What are the corticosteroids (and dosages) used as secondary treatments for adult anaphylaxis?

A
  • Hydrocortisone 250 mg IV
  • Methylprednisolone 80 mg IV
66
Q

What are the corticosteroids (and dosages) used as secondary treatments for pediatric anaphylaxis?

A
  • Hydrocortisone 50-100 mg IV
  • Methylprednisolone 2 mg/kg IV
67
Q

What causes Graves disease?

A

Autoantibodies to TSH receptor

68
Q

What is affected by the immune response characteristic of SLE?

A

RBCs, WBCs, nucleic acids, platelets, coag proteins

69
Q

What is/are the cause(s) of hereditary angioedema?

A

C1 Esterase inhibitor deficiency/dysfunction → excessive bradykinin production.

70
Q

What factors can cause C1 esterase problems?

A
  • Menses
  • Trauma
  • Infection
  • Stress
  • Oral contraceptives
71
Q

What typically limits the production of excessive bradykinin?

A

C1

C1 limits kallikrein and Factor XIIa.

72
Q

What occurs anatomically with excessive bradykinin?

A
  • Laryngeal swelling
  • Vasodilation
73
Q

What dose of antihistamine should be used for hereditary angioedema?

A

Trick question. Hereditary Angioedema = excessive bradykinin and is unaffected by antihistamines.

74
Q

What body parts are typically effected by hereditary angioedema?

A

Legs, hands, face, upper resp tract

75
Q

What is the typical cause of acquired angioedema?

A
  • ACE Inhibitors
76
Q

What symptoms are conspicuously absent with acquired angioedema?

A

No Urticaria or Pruritus

77
Q

What is responsible for the breakdown of bradykinin?

A

ACE

Thus ACE inhibitors = ↑ bradykinin = angioedema.

78
Q

What are the treatments for Angioedema?

A
  • Airway maintenance
  • FFP
  • C1 Inhibitor concentrate
  • Epinephrine
  • Antihistamines
  • Glucocorticoids?
79
Q

What cells are destroyed by the HIV virus?

A

Monocytes/Macrophages and T-cells

80
Q

How long does seroconversion take after inoculation with the HIV virus?

A

2-3 weeks

81
Q

What are the initial signs and symptoms of HIV conversion to AIDS?

A

Weight loss and failure to thrive

82
Q

How is HIV/AIDS diagnosed?

A
  • ELISA: 4-8 weeks after infection
  • Viral Load
  • CD4/Helper T lymphocytes < 200k
  • HAART agent sensitivity
83
Q

Inhibition of the liver’s ________ has huge implications for anesthetic delivery in HIV/AIDS patients.

A

CYP 450’s

84
Q

What s/s characterize scleroderma?

A
  • Inflammation
  • Vascular Sclerosis
  • Fibrosis of skin/viscera
85
Q

At what age does scleroderma typically occur?
What gender is typically affected?

A
  • 20-40
  • Females
86
Q

What GI symptoms of scleroderma are particularly pertinent to anesthesia?

A
  • GI Tract Hypomotility
  • ↓ LES tone
87
Q

______ fibrosis and ______ artery stenosis are prominent considerations for anesthesia in scleroderma patients.

A

Pulmonary fibrosis and renal artery stenosis

88
Q

What are the overall anesthesia implications of scleroderma?

A
  • Arterial catheter issues
  • Contracted intravascular volume
  • Aspiration risk
  • Limited neck mobility
  • ↓ pulmonary compliance
89
Q

What do inhalation agents do the immune system?

A
  • Suppress NK cells
  • Induce apoptosis of T-cells
  • Impair phagocytes

Unclear effects on tumor cells.

90
Q

This benzodiazepine, ________, decreases the migration of neutrophils.

A

Midazolam

91
Q

This induction agent, _______, will depress natural killer cell activity.

A

Ketamine

92
Q

This induction agent, ________, decreases cytokines but promotes NK cells.

A

Propofol

93
Q

What drug class will suppress NK cells?

A

Opioids

Particularly morphine and fentanyl.

94
Q

What cell type plays the greatest role in chronic inflammation?

A

T-Cells

95
Q

What cell type activates IgE and produces interleukins and interferons?

A

T-Cells

JW: Principles II (28 decks)

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