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Anesthesia Concepts 4 (Butera) > Immune > Flashcards

Immune Flashcards

1
Q

Innate/Natural Immune System

A

Limited specificity
immediate reaction
does not improve
no memory

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2
Q

Acquired/adaptive immune system

A

highly specific
develops in several days
Improves after exposure
has memory

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3
Q

cellular components of the natural immune system

A

granulocytes
monocytes/macrophages
natural killer cells
dendritic cells
mast cells

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4
Q

cellular components of the acquired immune system

A

CD4+ (helper) T cells
CD8+ (cytotoxic) T cells
B cells
plasma cells

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5
Q

Humoral components of the natural immune system

A

complement proteins
cytokines
acute phase proteins
antimicrobial proteins

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6
Q

Humoral components of the acquired immune system

A

antibodies

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7
Q

Possible modulators of immune competence during anesthesia and surgery

A
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8
Q

Volatile Anesthetics and Immune Response

A
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9
Q

Neutrophils

A

Fight bacterial and fungal infections

Most abundant type of WBC’s (60%)

Circulating neutrophils are rapidly primed to extravasate and migrate toward a site of inflammation/infection.

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10
Q

Monocytes

A

Circulating cells of the phagocyte system enter tissue and mature into macrophages

Phagocytosis
Release cytokines
Present pathogens to T-lymphocytes

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11
Q

Macrophages

A

Macrophages aretissue-resident or infiltrated immune cells critical for innate immunity, normal tissue development, homeostasis, and repair of damaged tissue.

Macrophage function is a sum of the local environment in which they reside, and the type of injuries or pathogen to which they are exposed

Often the first responders to infection, sending recruitment signals to other effector cells

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12
Q

Natural Killer Cells

A

Natural killer cellsprovide first line of defense against many viruses
Natural Killer (NK) Cells or large granular lymphocytes

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13
Q

____ develop in bone marrow and are potent killers of virus infected self cells

A

natural killer cells

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14
Q

____ are the main immune cells of the pregnant uterus, protects fetus against viral infections

A

natural killer cells

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15
Q

volatile anesthetics effect on immune cells (literature)

A

In vitrostudies revealed suppressive effects of volatile anesthetics on peripheral blood mononuclear cells(PBMCs) and macrophages

Sevoflurane and isoflurane at concentrations of 1.5 to 2.5 MAC suppressed the release of interleukin-1β and tumor necrosis factor(TNF)-α from human peripheral mononuclear cells stimulated by NK–sensitive tumor cells\

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16
Q

the role of platelets in fighting infection

A

Platelets have significant role in modulating clot formation
Additionally, they have considerable roles in inflammation and immune response
Gather at the damaged cite and adhere to white blood cells - release cytokines and chemokines which are chemotactic for neutrophils and monocytes.

Therefore, platelets are necessary for targeting lymphocytes, neutrophils and monocytes to inflammation site. Those interactions enhance inflammation

Serve as an immune cell by engulfing microbes

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17
Q

platelets and volatile anesthetics

A

Although the results of many studies have been conflicting, it appears that halothane, sevoflurane, and propofol inhibit platelet function in a reversible and dose-related manner at concentrations used clinically

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18
Q

Microglia

A

Resident cells of the brain that regulate brain development, maintenance of neuronal networks, and injury repair
Serve as brain macrophages but are distinct from other tissue macrophages owing to their unique homeostatic phenotype and tight regulation by the CNS microenvironment

They are responsible for the elimination of microbes, dead cells, redundant synapses, protein aggregates, and other particulate and soluble antigens that may endanger the CNS

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19
Q

Microglia and anesthesia

A

Inhaled anesthetics have been demonstrated to cause neuroinflammation by activating microglia and may be involved in perioperative neurocognitive disorders

Etomidate induces PND attributed to hippocampal microglial activation during the early pathological stage

Propofol has no effects on neuroinflammation and cognition in the Alzheimer’s transgenic model

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20
Q

Development of B-cells begins in _____.

A

bone marrow and is completed in lymph tissue.

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21
Q

B cells

A

When a mature B cell encounters and binds antigen, it proliferates and differentiates into plasma cells that secrete soluble antibodies directed against the antigen

The secreted antibodies are Ig molecules and members of the gamma globulin fraction of serum proteins

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22
Q

Humoral Response to Antigen

A

B-cell binds to antigen
Secretes soluble antibodies directed against that antigen
The secreted antibodies are immunoglobulin (Ig) molecules
There are five main classes: IgA, IgD, IgE, IgG, and IgM

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23
Q

IgA

A

Found in mucous, saliva, tears, and breast milk. Protects against pathogens.

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24
Q

IgD

A

Part of the B cell receptor. Activates basophils an d mast cells.

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25
Q

IgE

A

Protects against parasitic worms. Responsible for allergic reactions.

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26
Q

IgG

A

Secreted by plasma cells in the blood. Able to cross the placenta into the fetus.

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27
Q

IgM

A

May be attached to the surface of a B cell or secreted into the blood. Responsible for the early stages of immunity.

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28
Q

The location of the different antibodies

A

IgG comprises 70% of serum immunoglobulin
IgA 20%
IgM 10%
Low levels of IgE found primarily on mast cells and circulating basophils
IgD located on B-cell surfaces where it binds antigens

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29
Q

Lymphocytes

A

Acquired immunity depends on lymphocytes
Two main families B Lymphocytes (B-cells)and T Lymphocytes (T-cells)
B-cells are responsible for humoral immunity, which is provided by soluble antibodies directed at a specific antigen
T-cells are responsible for cell mediated immunity directed at a specific antigen

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30
Q

Helper type 1 T cells (CD4)

A

Th1 promote function of mononuclear phagocytes, produce interferon, and promote cell mediated immune responses

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31
Q

Helper type 2 (CD4)

A

Th2 promote function of B-lymphocytes, produce specific interleukins (IL- 4 and 10) which suppress cell mediated immunity

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32
Q

Cytotoxic T cells (CD8)

A

Induction of apoptosis in infected or tumor cells

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33
Q

Human Leukocyte Antigen (HLA)

A

Major histocompatibility complex(MHC) is a group of polymorphic genes expressed in nearly all the vertebrates, which determines histocompatibility between different individuals.

In humans MHC is known as HLA

Genetic variability in HLA type influences susceptibility to infection and autoimmune disease and rejection of transplanted tissue.

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34
Q

Eosinophils

A

Provide defense against parasitic infections and phagocytosis of allergen-antibody complexes formed in an allergic response

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35
Q

Mast Cells and Basophils

A

Essential component of hypersensitivity reactions

Release histamine, leukotrienes, and prostaglandins
Epinephrine prevents degranulation by binding to beta 2 receptors on the cell membrane

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36
Q

Monoclonal Antibodies

A

Abciximab (RePro) against clotting receptor glycoprotein IIb-IIIa on platelets
Adalimumab (Humira) against TNF alpha for RA
Alemtuzumab against an antigen on T and B lymphocytes to treat CLL
Basiliximab (Simulect) Used for acute kidney transplant rejection
Daclizumab (Zinbryta) For the treatment of MS
Etanercept (Enbrel) TNF inhibitor for RA
Infliximab (Flixabi) used for crohns and RA
Omalizumab (Xolair) Binds to IgE receptor on the surface of mast cells used for treatment of asthma

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37
Q

Monoclonal Antibodies to treat COVID

A

Treatment pills: Paxlovid & Molnupiravir
Injections/Infusions: Remdesivir & Bebtelovimab

Sotrovimabis a monoclonal antibody that is specifically directed against the spike protein of SARS-CoV-2 and is designed to block the virus’ attachment and entry into human cells. FDA no longer authorized where BA.2 subvariantpredominates

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38
Q

Human Immunodeficiency Virus

A

Secondary immunosuppression can result from infection that causes depletion of immune cells

The primary target of HIV infection is CD4 lymphocytes Normal CD4 is 500-1500
Below 200 from advanced HIV infection is diagnosed with AIDS

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39
Q

Treatment of HIV

A

Highly Active Antiretroviral Therapy (HARRT) has been effective in stopping HIV replication and has changed HIV to a chronic manageable disease

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40
Q

Anesthesia Management of HIV

A

There is no conclusive evidence to support any recommendations

Protease inhibitors (amprenavir, indinavir ritonavir, saquinavir and tipranavir) decrease the metabolic pathways of opioids, nonsteroidal anti-inflammatory drugs, lidocaine and benzodiazepines

Careful titration of midazolam and fentanyl as the effects may be enhanced
Continue antiretroviral therapy

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41
Q

Different medications and their effect on patients with HIV

A

Midazolam - prolonged action after saquinavir
Fentanyl can have prolonged action as well
Prolonged effect after Non depolarizer muscle relaxants
Enhanced hypotensive effects after calcium channel blockers

42
Q

Viral load and CD4 count for patients with HIV

A

Viral load and CD4+ count: mortality is inversely related to CD4+ count

Viral load is the term used to describe the amount of HIV in the patients blood, the higher your viral load, then the faster your CD4 cell count will fall, and the greater your risk of becoming ill because of HIV

43
Q

Occupational Risk of caring for patients with HIV

A

Percutaneous injury with a hollow-bore needle is the most common mechanism of occupational HIV transmission

The average risk of HIV transmission associated with exposure to HIV infected blood is 0.3% after needle-stick injury and 0.09% after mucous membrane exposure

44
Q

Post HIV Exposure Prophylaxis

A

The CDC recommends PrEP with antiretroviral medications soon after occupational exposure within hours and administered for 4 weeks

45
Q

Four types of allergic reactions

A

Type I….Immediate
Type II….cytotoxic
Type III…..Immune complex
Type IV…..delayed cell mediated

46
Q

Type I Reaction

A

Rapidly developing reaction that results from antigen-antibody interaction in an individual who has been previously exposed

Histamine stored in mast cells and basophils is released when an allergen interacts with membrane bound IgE

47
Q

Anaphylactoid Reaction

A

Anaphylactoid reactions are caused by histamine release from basophils and mast cells in response to non-IgE mediated triggering event

Reactions are similar but less severe
No prior exposure is needed

48
Q

Pathophysiology of anaphylaxis vs anaphylactoid reactions

A

anaphylaxis- IgE mediated reaction = urticaria, hypotension, bronchospasm and requires prior exposure

anaphylactoid- non-IgE mediated reaction, can appear identical to anaphylaxis but doesn’t require prior exposure (for example IV iodine contrast)

49
Q

Defining an anaphylactic reaction (Qs to ask)

A

Is sensitization required? YES
Can reaction occur on first exposure? NO
How much exposure is needed to elicit a reaction? VERY LITTLE
Is reaction predicted by allergy skin tests? YES

50
Q

Defining an anaphylactoid reaction (Qs to ask)

A

Is sensitization required? NO
Can reaction occur on first exposure? YES
How much exposure is needed to elicit a reaction? Usually more then for anaphylaxis

Is reaction predicted by allergy skin tests? NO

51
Q

Histamine

A

Produces the symptoms of allergic reactions
H1 receptors
Vasodilation, Increased vascular permeability, and contraction of smooth muscle other than blood vessels
H2 receptors
Cardiac stimulation, Stimulation of gastric secretions

52
Q

Arachidonic Acid Metabolites

A

Leukotrienes and Prostaglandins are proinflammatory mediators resulting from metabolic degradation of the arachidonic acid originating from membrane phospholipids

Bronchoconstriction and vasodilatation

53
Q

Tryptase

A

Tryptase is a marker for an allergic reaction. It is released with histamine from the mast cells and has a peak blood level 15-120 minutes after exposure.

54
Q

Grade I =

A

Cutaneous
Erythema Pruritus Urticaria with or without Angioedema

55
Q

Grade II =

A

Cutaneous Grade I signs
Cardiovascular
Hypotension Tachycardia Pre-syncope
Respiratory
Dyspnea
Wheezing
Gastrointestinal
Nausea Vomiting Diarrhea Abdominal pain

56
Q

Grade III =

A

Cardiovascular Grade II signs plus Cardiovascular collapse Profound hypotension Bradycardia Dysrhythmia
Respiratory
Bronchospasm
Hypoxia (Sao2 < 92%) Gastrointestinal
Grade II signs plus
Incontinence
Neurologic
Confused Unconscious

57
Q

Grade IV =

A

Cardiovascular
Pulseless electrical activity Cardiac arrest

58
Q

Treatment for anaphylaxis reactions

A

All drugs and surgery should be stopped
Airway patency must be maintained and 100% oxygen given
Titrate dose according to the severity of symptoms and patient response
Repeat dose every 1-2 minutes if necessary
Adults Children
Grade 2: 10-20 mcg 1-5mcg/kg
Grade 3: 100-200 mcg 1-5 mcg/kg
Grade 4: 1 mg 10mcg/kg

59
Q

The β-adrenergic properties of epinephrine cause ______

A

bronchodilation, increase myocardial output and contractility, and suppress further mediator release from mast cells and basophils

60
Q

What to do if the patient is refractory to epinephrine….

A

Vasopressin: IV doses 2-10 IU until response
Norepinephrine 0.05-0.1 mcg/kg/min
Diphenhydramine 0.5-1 mg/kg IV (H1 antagonist)
H2 receptor antagonist (Ranitidine)
Hydrocortisone adult 250mg IV, children 50-100mg
Bronchodilators Inhaled albuterol

61
Q

Agents responsible for perioperative Allergic Reactions

A

Neuromuscular Blocking agents: 47.4%
Latex: 20%
Antibiotics: 18% (beta-lactems)
Hypnotics: 1%
Opioids: 2%
Colloids: 2%
Protamine, contrast media and others: 9%
Local Anesthetics: 0.6%

62
Q

Neuromuscular blocking drugs

A

Common cause of perioperative allergic reactions
Antigenic quaternary ammonium groups
Rocuronium, vecuronium, and pancuronium have single quaternary ammonium group are less likely to cause anaphylaxis
Most common NMBD to cause anaphylaxis is succinylcholine

62
Q

Agents responsible for perioperative Allergic Reactions

A

Neuromuscular Blocking agents: 47.4%
Latex: 20%
Antibiotics: 18% (beta-lactems)
Hypnotics: 1%
Opioids: 2%
Colloids: 2%
Protamine, contrast media and others: 9%
Local Anesthetics: 0.6%

63
Q

List the neuromuscular blocking agents from highest to lowest incidence of allergy

A

Succinylcholine> atracurium> cisatracurium> rocuronium> vecuronium

64
Q

Latex allergy

A

Latex allergy is recognized as a significant problem for healthcare workers and patients

Latex allergy is a IgE-mediated reaction

General population has a low incidence 1% to 2%

65
Q

Who are high risk groups for latex allergies?

A

Healthcare workers with frequent latex glove use (8-16%)
Children with spina bifida, spinal cord trauma and urogenital malformations or any patient with repeated exposure to latex for any reason (24-64%)

66
Q

Which food allergies increase the risk for latex allergy?

A

Avocado
Mango
Banana
Pineapple
Tomato
Papaya
Chestnuts
Kiwi

67
Q

Symptoms of Latex Allergy

A

Immediate (Type I) hypersensitivity IgE mediated occurs 5-30 minutes after initial contact

Delayed (Type IV) hypersensitivity within 6-48 hours after initial contact

Contact dermatitis, non allergic occurring in frequent glove users

68
Q

Biphasic Anaphylaxis

A

Delayed reaction (6 Hrs)
Theories of pathogenesis-The pathogenesis of biphasic anaphylaxis is not known, although several theories have been proposed

Influx of inflammatory cells
Second wave of mast cell degranulation
Late synthesis of platelet-activating factor
Effects of therapies “wearing off”
Uneven antigen absorption
Inadequate or delayed epinephrine

69
Q

Type II Reactions

A

Cytotoxic Reactions also known as antibody-mediated cytotoxic hypersensitivity

Mediated by IgG or IgM

ABO incompatibility, autoimmune hemolytic anemia and myasthenia gravis, Goodpasture syndrome are examples of type II hypersensitivity reactions

70
Q

Myasthenia Gravis

A

Autoimmune disorder

Fatigable skeletal muscle weakness

Antibody mediated attack of acetylcholine receptor in the post synaptic membrane of the neuromuscular junction

71
Q

Difference between myasthenia gravis and Lambert Eaton synrome

A

Myasthenia Gravis:
antibody against AchR antibody
associated with thymic tumor
weakness worsens on prolonged exercise
normal deep tendon reflexes
autonomic dysfunction is present on repeated nerve stimulation, there is decremental response

Lambert Eaton Sydrome:
antibody against voltage gated calcium channel
associated with small lung cell CA
weakness improves with prolonged exercise
decreased or absent deep tendon reflexes
autonomic dysfunction is present
On repeated nerve stimulation, there is incremental response

72
Q

Anesthesia considerations for myasthenia gravis

A

Continue anticholinesterase agents up to and including the am of surgery

Patients are sensitive to nondepolarizing and resistant to succinylcholine

Unpredictable response to NMBA reversal

73
Q

Type III Reaction

A

Type III reactions represent immune complex diseases that result from antigen and antibodies that bind to insoluble complexes in the microvasculature
Complement is activated and neutrophils are localized to the site

Immune complex diseases include systemic lupus, rheumatoid arthritis, and glomerulonephritis are examples

74
Q

Rheumatoid Arthritis

A

An autoimmune disease that targets the synovial joints. Systemic involvement due to infiltration of immune complexes into small arteries leading to vasculitis
Cytokines TNF and Interleukin-1 play a central role
2-3 times more common in women

75
Q

Complications of Rheumatoid Arthritis

A

Airway:
TMJ synovitis-limited mouth opening

Cricoarytenoid arthritis- narrow glottis opening

AO instability- risk of spinal cord and vertebral artery compression

76
Q

Anti-rheumatic drugs

A

Drugs inhibit TNF, IL 1 and 6 and inhibit T cells and B cells.

All drug suppress the immune system and risk infection and cancer
Methotrexate, cyclosporine and Enbrel (etanercept)
Methotrexate causes liver dysfunction and suppresses bone marrow function
Cyclosporine increases the duration of succinylcholine

77
Q

Systemic Lupus Erythematosus

A

An autoimmune disorder characterized by proliferation of antinuclear antibodies
SLE affects every organ system as a result of antibody induced vasculitis
SLE is a disease that targets young women

78
Q

Complications of lupus

A

Cricoarytenoiditis and recurrent laryngeal nerve palsy
Restrictive pulmonary defect, pleural effusion and PE
Pericarditis, Raynaud’s, Hypertension
Hypercoagulability, thrombocytopenia, anemia

79
Q

Anesthetic considerations for lupus

A

Hoarseness and stridor could indicate cricoarytenoids arthritis, risk of post-extubation laryngeal swelling and airway obstruction. Consider smaller ETT
PTT may be prolonged but hypercoagulability increases risk of stroke DVT and PE
Cyclophosphamide inhibits plasma cholinesterase and increases duration of succinylcholine
Pregnancy, stress, infection and surgery can exacerbate symptoms

80
Q

What exacerbates lupus?

A

PISSED CHIMP
Pregnancy, Infection, Surgery, Stress, Enalipril, D-penicillamine

Captopril, Hydralazine, Isoniazid, Methyldopa, Procainamide

81
Q

Type IV Reactions

A

Delayed Hypersensitivity Reactions
Antigen specific lymphocyte binding produces cytokine release and a local inflammatory response
Manifest in 18-24 hours
Peak 40-80 hours
Duration of 72-96 hours
Graft verses host reactions and contact dermatitis

82
Q

Types of Hypersensitivity Reactions

A
83
Q

Surgery stimulates the stress response which causes the release of ____

A

cortisol and catecholamines

84
Q

Perioperative ____ commonly occurs

A

lymphopenia

85
Q

Stress reduces what ratio?

A

Stress reduces the Th1/Th2 ratio and predisposes patients to infection

86
Q

Impaired lymphocyte proliferation may be caused by _____

A

circulating factors (stress hormones) and IV and inhalational agents

87
Q

Tissue injury causes _____

A

a localized response by cells, innate system releases macrophages
IL-1 and TNF released from resident macrophages stimulate IL-6
IL-6 stimulates hepatocytes to release acute phase proteins (c-reactive proteins CRP)
Magnitude of this increase correlates with the intensity of the procedure
CRP may be predictive of perioperative mortality

88
Q

Propofol does what to the immune system?

A

reduces inflammatory mediator levels, monocyte phagocytosis, oxidative burst, NOS production, and chemotaxis, neutrophil chemotaxis, release of superoxide and elastase

89
Q

Dexmedetomidine does what to the immune system?

A

Reduces pro-inflammatory cytokine levels and neutrophil chemotaxis

90
Q

Ketamine does what to the immune system?

A

Reduces systemic pro-inflammatory cytokine levels, and monocyte production of NO
Impairs neutrophil adhesion, degranulation, and antioxidant activity, as well as platelet aggregation
Increases Th1/Th2 ratio and improves immune function, but does not alter NK cell action

91
Q

Sevoflurane does what to the immune system?

A

Decrease neutrophil oxidative burst, chemotaxis, and cytokine secretion

92
Q

Desflurane does what to the immune system?

A

Genotoxic and pro-inflammatory effects in minor surgery

93
Q

Benzodiazepine do what to the immune system?

A

Inhibit neutrophil and mast-cell activation

Reduce pro-inflammatory cytokine secretion

Induce an anti-inflammatory M2 monocyte/macrophage phenotype

94
Q

Opioids do what to the immune system?

A

Block macrophage chemotaxis and phagocytosis
Decrease neutrophil bactericidal action
Direct T cells toward Th2 differentiation

Morphine suppresses NK cells

95
Q

Regional anesthesia does what to the immune system?

A

Reduce neutrophil activation, decrease macrophages migration to the site of injury bactericidal effects, increase the integrity of endothelial barrier

Spinal and epidural anesthesia have been found to prevent postoperative leukopenia and adverse changes in lymphocyte sub-populations and NK-cell activity that occur in patients undergoing GA and surgery

96
Q

Systemic Inflammatory Response Syndrome

A

SIRS Criteria, 2 or more signs
Temp > 38 C or < 36 C
HR > 90, RR > 20 or PaCO2 < 32 mmHg
WBC >12,000 or <4000 or >10% immature forms

Diagnosis: Based on confirmation of specific causative organism

97
Q

Sepsis categories

A

Sepsis Criteria = suspected or present source of infection

Severe Sepsis Criteria = Lactic acidosis, SBP , 90 or > 40 mmHg drop from baseline

Septic shock = Severe sepsis with hypotension despite adequate fluid resuscitation

98
Q

Treatment and Prognosis of Sepsis

A

Treatment Broad spectrum antibiotics and supportive care for failing organs

Prognosis: Depends on the virulence of the infecting organism, the time when therapy is started, the inflammatory response of the patient, the immune status of the patient, and the extent of organ system dysfunction

99
Q

Management of Sepsis

A

Preoperative: Postpone surgery if possible surgery may be required for bowel perforation or to remove the infection source.
Antibiotics may be the intervention that can alter the course of the disease
Postoperative usually ICU after surgery intubated

100
Q

Surviving Sepsis Campaign 2021

A

For patients with sepsis- induced hypoperfusion or septic shock at least 30 mL/kg of IV crystalloid fluid should be given within the first 3 hours of resuscitation.
For adults with sepsis or septic shock, balanced crystalloid instead of normal saline for resuscitation.

101
Q

Guidelines for treating sepsis

A

Vasopressors peripherally to restore mean arterial pressure rather than delaying initiation until a central venous access is secured.
Sepsis or septic shock we suggest against using IV vitamin C.
Septic shock and an ongoing requirement for vasopressor therapy followed by IV corticosteroids.

30 mL/kg IV crystalloid. This recommendation was downgraded from a strong recommendation to a weak recommendation based on the low quality of evidence.
Antimicrobials as soon as possible, ideally within 1 hour of sepsis recognition. (no Change)
For adult survivors of sepsis or septic shock, recommend assessment and follow-upfor physical, cognitive, and emotional problems after hospital discharge

Anesthesia Concepts 4 (Butera) (15 decks)

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